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Dual and Opposing Functions of the Central Amygdala in the Modulation of Pain.
Cell Reports ( IF 7.5 ) Pub Date : 2019-10-08 , DOI: 10.1016/j.celrep.2019.09.011
Torri D Wilson 1 , Spring Valdivia 1 , Aleisha Khan 1 , Hye-Sook Ahn 1 , Anisha P Adke 1 , Santiago Martinez Gonzalez 1 , Yae K Sugimura 1 , Yarimar Carrasquillo 1
Affiliation  

Pain perception is essential for survival and can be amplified or suppressed by expectations, experiences, and context. The neural mechanisms underlying bidirectional modulation of pain remain largely unknown. Here, we demonstrate that the central nucleus of the amygdala (CeA) functions as a pain rheostat, decreasing or increasing pain-related behaviors in mice. This dual and opposing function of the CeA is encoded by opposing changes in the excitability of two distinct subpopulations of GABAergic neurons that receive excitatory inputs from the parabrachial nucleus (PB). Thus, cells expressing protein kinase C-delta (CeA-PKCδ) are sensitized by nerve injury and increase pain-related responses. In contrast, cells expressing somatostatin (CeA-Som) are inhibited by nerve injury and their activity drives antinociception. Together, these results demonstrate that the CeA can amplify or suppress pain in a cell-type-specific manner, uncovering a previously unknown mechanism underlying bidirectional control of pain in the brain.



中文翻译:

中央杏仁核在疼痛调节中的双重和对立功能。

疼痛感对于生存至关重要,可以被期望,经验和环境所放大或抑制。疼痛的双向调节的神经机制仍然是未知的。在这里,我们证明杏仁核(CeA)的中央核起止痛剂的作用,减少或增加小鼠的疼痛相关行为。CeA的这种双重和相反的功能是通过从臂旁神经核(PB)接收兴奋性输入的GABA能神经元的两个不同亚群的兴奋性的相反变化来编码的。因此,表达蛋白激酶C-δ(CeA-PKCδ)的细胞会因神经损伤而变得敏锐,并增加与疼痛相关的反应。相反,表达生长抑素(CeA-Som)的细胞会受到神经损伤的抑制,其活性会驱动抗伤害感受。一起,

更新日期:2019-10-10
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