TY - JOUR
T1 - Brain circuits mediating opposing effects on emotion and pain
AU - Cai, You Qing
AU - Wang, Wei
AU - Paulucci-Holthauzen, Adriana
AU - Pan, Zhizhong Z.
N1 - Publisher Copyright:
© 2018 the authors.
PY - 2018/7/11
Y1 - 2018/7/11
N2 - The amygdala is important for processing emotion, including negative emotion such as anxiety and depression induced by chronic pain. Although remarkable progress has been achieved in recent years on amygdala regulation of both negative (fear) and positive (reward) behavioral responses, our current understanding is still limited regarding how the amygdala processes and integrates these negative and positive emotion responses within the amygdala circuits. In this study with optogenetic stimulation of specific brain circuits, we investigated how amygdala circuits regulate negative and positive emotion behaviors, using pain as an emotional assay in male rats. We report here that activation of the excitatory pathway from the parabrachial nucleus (PBN) that relays peripheral pain signals to the central nucleus of amygdala(CeA) is sufficient to cause behaviors of negative emotion including anxiety, depression, and aversion in normal rats. In strong contrast, activation of the excitatory pathway from basolateral amygdala (BLA) that conveys processed corticolimbic signals to CeA dramatically opposes these behaviors of negative emotion, reducing anxiety and depression, and induces behavior of reward. Surprisingly, activating the PBN–CeA pathway to simulate pain signals does not change pain sensitivity itself, but activating the BLA–CeA pathway inhibits basal and sensitized pain. These findings demonstrate that the pain signal conveyed through the PBN–CeA pathway is sufficient to drive negative emotion and that the corticolimbic signal via the BLA–CeA pathway counteracts the negative emotion, suggesting a top-down brain mechanism for cognitive control of negative emotion under stressful environmental conditions such aspain.
AB - The amygdala is important for processing emotion, including negative emotion such as anxiety and depression induced by chronic pain. Although remarkable progress has been achieved in recent years on amygdala regulation of both negative (fear) and positive (reward) behavioral responses, our current understanding is still limited regarding how the amygdala processes and integrates these negative and positive emotion responses within the amygdala circuits. In this study with optogenetic stimulation of specific brain circuits, we investigated how amygdala circuits regulate negative and positive emotion behaviors, using pain as an emotional assay in male rats. We report here that activation of the excitatory pathway from the parabrachial nucleus (PBN) that relays peripheral pain signals to the central nucleus of amygdala(CeA) is sufficient to cause behaviors of negative emotion including anxiety, depression, and aversion in normal rats. In strong contrast, activation of the excitatory pathway from basolateral amygdala (BLA) that conveys processed corticolimbic signals to CeA dramatically opposes these behaviors of negative emotion, reducing anxiety and depression, and induces behavior of reward. Surprisingly, activating the PBN–CeA pathway to simulate pain signals does not change pain sensitivity itself, but activating the BLA–CeA pathway inhibits basal and sensitized pain. These findings demonstrate that the pain signal conveyed through the PBN–CeA pathway is sufficient to drive negative emotion and that the corticolimbic signal via the BLA–CeA pathway counteracts the negative emotion, suggesting a top-down brain mechanism for cognitive control of negative emotion under stressful environmental conditions such aspain.
KW - Amygdala
KW - Brain circuits
KW - Emotion
KW - Optogenetics
KW - Pain
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UR - http://www.scopus.com/inward/citedby.url?scp=85051062150&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.2780-17.2018
DO - 10.1523/JNEUROSCI.2780-17.2018
M3 - Article
C2 - 29941444
AN - SCOPUS:85051062150
SN - 0270-6474
VL - 38
SP - 6340
EP - 6349
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 28
ER -