神经科学
谷氨酸的
痛觉超敏
谷氨酸受体
扣带回前部
体感系统
医学
神经损伤
心理学
痛觉过敏
伤害
内科学
受体
认知
作者
Xia Zhu,Hao-Di Tang,Wanying Dong,Fang Kang,An Liu,Yu Mao,Wen Xie,Shouxin Zhang,Peng Cao,Wenjie Zhou,Haitao Wang,Zahra Farzinpour,Wenjuan Tao,Xiaoyuan Song,Yan Zhang,Tian Xue,Yan Jin,Juan Li,Zhi Zhang
标识
DOI:10.1038/s41593-021-00811-x
摘要
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.
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