中国科学技术大学张智、李娟和晋艳研究团队合作取得一项新成果。他们发现，不同的丘脑皮质回路是由组织损伤和抑郁样状态引起的异常性疼痛的基础。相关论文发表在2021年3月8日出版的《自然-神经科学》杂志上。
他们确定了雄性小鼠中的两个离散的谷氨酸能神经元回路：从丘脑后核（POGlu）到原代体感皮层的谷氨酸能神经元（S1Glu）的投射介导了组织损伤引起的异常性疼痛，是从束旁丘脑核（PFGlu）到途径前扣带回皮层中含有GABA的神经元，再到谷氨酸能神经元（ACCGABA→Glu）介导与抑郁样状态相关的异常性疼痛。
体内钙成像和多四极电生理记录表明，在两种情况下，POGlu和PFGlu群体经历了不同的适应。每个回路的人工操作都会影响由组织损伤或抑郁状态引起的异常性疼痛，但不会同时影响两者。
他们的研究表明，不同的丘脑皮质回路POGlu→S1Glu和PFGlu→ACCGABA→Glu分别能减轻与组织损伤和抑郁样状态相关的异常性疼痛，从而为了解不同病因引起的病理性疼痛的回路基础提供了见解。
据了解，在人体中，组织损伤和抑郁症均可引起疼痛超敏反应，但是尚不清楚是否涉及不同的回路。
附：英文原文
Title: Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states
Author: Xia Zhu, Hao-Di Tang, Wan-Ying Dong, Fang Kang, An Liu, Yu Mao, Wen Xie, Xulai Zhang, Peng Cao, Wenjie Zhou, Haitao Wang, Zahra Farzinpour, Wenjuan Tao, Xiaoyuan Song, Yan Zhang, Tian Xue, Yan Jin, Juan Li, Zhi Zhang
Issue&Volume: 2021-03-08
Abstract: In humans, tissue injury and depression can both cause pain hypersensitivity, but whether this involves distinct circuits remains unknown. Here, we identify two discrete glutamatergic neuronal circuits in male mice: a projection from the posterior thalamic nucleus (POGlu) to primary somatosensory cortex glutamatergic neurons (S1Glu) mediates allodynia from tissue injury, whereas a pathway from the parafascicular thalamic nucleus (PFGlu) to anterior cingulate cortex GABA-containing neurons to glutamatergic neurons (ACCGABA→Glu) mediates allodynia associated with a depression-like state. In vivo calcium imaging and multi-tetrode electrophysiological recordings reveal that POGlu and PFGlu populations undergo different adaptations in the two conditions. Artificial manipulation of each circuit affects allodynia resulting from either tissue injury or depression-like states, but not both. Our study demonstrates that the distinct thalamocortical circuits POGlu→S1Glu and PFGlu→ACCGABA→Glu subserve allodynia associated with tissue injury and depression-like states, respectively, thus providing insights into the circuit basis of pathological pain resulting from different etiologies.
DOI: 10.1038/s41593-021-00811-x
Source: https://www.nature.com/articles/s41593-021-00811-x
Nature Neuroscience：《自然—神经科学》，创刊于1998年。隶属于施普林格·自然出版集团，最新IF：28.771
官方网址：https://www.nature.com/neuro/
投稿链接：https://mts-nn.nature.com/cgi-bin/main.plex
本期文章：《自然—神经科学》：Online/在线发表
