1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
|
{
"titles": [
"2008 - Rutter_s child and adolescent psychiatry-Blackwell Pub (2008).pdf",
"2013 - Neural-Immune Interactions in Brain Function and Alcohol Related Disorders.pdf",
"2010 - Candidate Gene and Genome-Wide Association Studies in Behavioral Medicine.pdf",
"2010 - Candidate Gene and Genome-Wide Association Studies in Behavioral Medicine.pdf",
"2007 - Gene expression profiles in anatomically and functionally distinct regions.pdf",
"2009 - Multiscale Genomic Analysis of the Corticolimbic System_ Uncoveri (1).pdf",
"2009 - Neuroplasticity, Psychosocial Genomics.pdf",
"2010 - Candidate Gene and Genome-Wide Association Studies in Behavioral Medicine.pdf",
"2010 - Candidate Gene and Genome-Wide Association Studies in Behavioral Medicine.pdf",
"2010 - Candidate Gene and Genome-Wide Association Studies in Behavioral Medicine.pdf"
],
"extraction_id": [
"5e06bd24-8977-582c-b01b-61be91612e1a",
"fb4ba6b4-c3ea-5671-9da8-15fcadccff59",
"d0222d2f-7e27-59de-9ad0-23febb3564f8",
"4d38ecad-88e4-5f52-8a99-55029773de79",
"b848d23b-0c65-5e44-b190-1ec8e5a76545",
"c755176c-961c-57f0-996c-662de89048d3",
"8cd38348-d367-5c85-829e-e465af8184cb",
"995b3eb6-e505-52a0-a142-ca507eb9a9ac",
"264526ff-3f41-5a6d-88af-6e237cea42cb",
"069a2a63-f01c-5235-a118-3744c21f2baa"
],
"document_id": [
"59daba11-206e-5bbc-8833-9d1b661532b5",
"78271275-3409-5fc7-bbdd-53c484178e0b",
"17637a6f-804e-50e4-9cf5-37318e17f15c",
"17637a6f-804e-50e4-9cf5-37318e17f15c",
"d4a001e2-8cac-58cb-be8b-b9afa9382e01",
"3d0df5a3-7d7c-5edc-b94d-cae582f59c12",
"77549d17-8f07-5b62-8134-011a68f2ebd4",
"17637a6f-804e-50e4-9cf5-37318e17f15c",
"17637a6f-804e-50e4-9cf5-37318e17f15c",
"17637a6f-804e-50e4-9cf5-37318e17f15c"
],
"id": [
"chatcmpl-ADZMeEIq2Wv2GICWJZcSZAU1k5Qdz",
"34f059bf-1e74-580d-9b52-8c940ff0f302",
"fd7b6e37-2aba-525e-aa22-4a9cef18827d",
"f2dda7e1-1af6-54b0-8ffa-856313872579",
"96a2a72c-b239-58f0-b116-2b1eeb3e8434",
"b2d814c0-e515-54b9-b994-b457ca0e2739",
"45e53d76-dced-5f6b-abf2-c830b41c1c90",
"2fc8ee5e-7a5e-57cc-98e3-e9156aec2571",
"fbdf5982-c2f0-5577-bce3-bc8762aef713",
"2199f4c4-8126-54c8-a323-6704c96bc0f7",
"8b65f73a-2d73-53b2-b418-f8e485d58df3"
],
"contexts": [
"areas that support pos-itive emotions and deactivate brain areas that are linked withaggression, fear and sadness (Diamond, 2004); this nding is consistent with the emotional prole associated with agreeableness.",
"Importantly, regions of the brain responsible for emotional regulation, executive functioning, and their consequential behavioral outcomes are sensitive to in ammation [ 22 ] . The extended limbic system, primitively responsible for fear and pleasure responses, stress, memory, and learning, has been shown to be modulated by immune signaling. Early work established that there is a high density of IL-1 receptors in the dentate gyrus and pyramidal cell layer of the hippocampus, the",
"the midbrain structures are implicated in cardiacresponses to social stress (Wager et al, 2009 ). It is now evident that these same brain regions are involved in emotion regulation. Furthermore, the circuitry involved in physical pain and plea-sure appears to be activated by positive and negative socially induced emotion (Takahashi et al, 2009 ). The possibility therefore arises that positive well-being may be embodied in the acti- vation of neural circuitry in a reciprocal fashion",
"723732. Etkin, A., Egner, T., Peraza, D. M., Kandel, E. R., and Hirsch, J. (2006). Resolving emotional conict: a rolefor the rostral anterior cingulate cortex in modulatingactivity in the amygdala. Neuron, 51 , 871882. Fales, C. L., Barch, D. M., Rundle, M. M., Mintun, M. A., Snyder, A. Z. et al (2008). Altered emotional inter-ference processing in affective and cognitive-controlbrain circuitry in major depression. Biol Psychiatry, 63, 377384. Fanselow, M. S. (2000). Contextual fear, gestalt mem-",
"for cognitive processes such as learning,memory, and emotions.",
"expression of emotional behavior. Sensory inputs with emotional components are transmitted to the amygdala where they are processed and fu rther relayed to other regions to modulate autonomic and behavioral responses, and to form emotional memories (LeDoux, 2000; Rosen, 2004). As a neural substrate of emotionality, many neuropsychiatric disorders have been associated with structural changes i n the amygdala. Individuals with genetically predisposed susceptibility to anxiety and depression have",
"components can act back upon its physical substrate. Thought, emotion, and action trigger neural activity, which can lead to a reorganization of the brain, shaping future psychosocial experience. From this perspective, we are not the passive products of neurophysiology and heredity; rather, through our behavior in the social environment, we become active agents in the con-struction of our own neurobiology and, ultimately, our own lives.",
"et al, 1995 ; Scher et al, 2005 ), (2) are less easily distracted from negative emotion process- ing (Ellenbogen et al, 2002 ; Lyubomirsky et al, 1998 ; Siegle et al, 2002 ; Wenzlaff and Bates, 1998 ), (3) show heightened stress hormone lev- els such as cortisol that may have deleterious effects on the brain (Sapolsky, 2000 ), and (4)",
"et al, 2000 ). Once activated, the amygdala sets in motion a cascade of responses to threat via pro-jections to the hypothalamus and prefrontal cor-tex (LeDoux, 1996 ). A neural region that is criti- cal for regulating responses to emotional stimuli is the ventrolateral prefrontal cortex (VLPFC;Hariri et al, 2002 ). Studies have shown that the labeling of negative affective states activates the right VLPFC and that increased activity inright VLPFC is associated with decreased activ-",
"tially participates in negative emotional states,although it also participates in positive emo- tional states (Zald, 2003 ). The amygdala orches- trates the somatomotor, visceral, and cognitiveresponses to threats by virtue of its connections with cortical brain structures above and hypotha- lamic and brainstem structures below it (LeDouxet al, 1990 ). The nucleus accumbens and ventral striatum participate in reward responses and pos- itive emotional states. Other structures that are"
],
"answer": "Our brains maintain emotions through a complex interplay of various brain regions and neural circuits. Key areas involved include: 1. **Amygdala**: Sensory inputs with emotional components are transmitted to the amygdala, where they are processed and further relayed to other regions to modulate autonomic and behavioral responses, and to form emotional memories [6]. The amygdala orchestrates responses to threats and is involved in both negative and positive emotional states [10]. 2. **Prefrontal Cortex**: The ventrolateral prefrontal cortex (VLPFC) is critical for regulating responses to emotional stimuli. Increased activity in the right VLPFC is associated with decreased activity in the amygdala, which helps in managing negative affective states [9]. 3. **Extended Limbic System**: This system, which includes structures like the hippocampus, is primitively responsible for fear and pleasure responses, stress, memory, and learning. It is modulated by immune signaling, indicating that inflammation can affect emotional regulation [2]. 4. **Midbrain Structures**: These structures are involved in emotion regulation and are activated by both physical pain and pleasure, as well as positive and negative socially induced emotions [3]. 5. **Nucleus Accumbens and Ventral Striatum**: These areas participate in reward responses and positive emotional states [10]. Overall, the brain maintains emotions through the coordinated activity of these regions, which process, regulate, and respond to emotional stimuli, thereby shaping our emotional experiences and behaviors.",
"question": "how do our brains maintain emotions"
}
|
