机制(生物学)
神经科学
神经元
内生
类阿片
内源性阿片
心理学
医学
内科学
受体
物理
量子力学
作者
Youjun Dou,Yuan Liu,Wen-Qun Ding,Qing Li,Hua Zhang,Ling Li,Mengting Zhao,Z. Li,Jing Yuan,Xiaofei Wang,Wangyuan Zou,Anan Li,Yingjie Sun
摘要
Abstract Endogenous opioid antinociception is a self-regulatory mechanism that reduces chronic pain, but its underlying circuit mechanism remains largely unknown. Here, we showed that endogenous opioid antinociception required the activation of mu-opioid receptors (MORs) in GABAergic neurons of the central amygdalar nucleus (CEA) in a persistent-hyperalgesia mouse model. Pharmacogenetic suppression of these CEAMOR neurons, which mimics the effect of MOR activation, alleviated the persistent hyperalgesia. Furthermore, single-neuron projection analysis revealed multiple projectome-based subtypes of CEAMOR neurons, each innervating distinct target brain regions. We found that suppressing of axon branches projecting to the parabrachial nucleus (PB) of one subtype of CEAMOR neurons alleviated persistent hyperalgesia, indicating a subtype- and axonal branch-specific mechanism of action. Further electrophysiological analysis revealed that suppression of a distinct CEA-PB disinhibitory circuit controlled endogenous opioid antinociception. Thus, this study identified the central neural circuit that underlies the endogenous opioid antinociception, providing new insight into the endogenous pain modulatory mechanisms.
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