谷氨酸的
神经科学
伏隔核
共病
丘脑
萧条(经济学)
SNi公司
加巴能
医学
慢性疼痛
神经损伤
上瘾
心理学
谷氨酸受体
精神科
生物
内科学
中枢神经系统
抑制性突触后电位
受体
宏观经济学
经济
水解
生物化学
酸水解
作者
Jie Deng,NULL AUTHOR_ID,Cuicui Liu,NULL AUTHOR_ID,NULL AUTHOR_ID,Jia‐You Wei,NULL AUTHOR_ID,Hai‐Ting Fan,NULL AUTHOR_ID,NULL AUTHOR_ID,NULL AUTHOR_ID,NULL AUTHOR_ID,NULL AUTHOR_ID,NULL AUTHOR_ID,Ting Xu,NULL AUTHOR_ID,NULL AUTHOR_ID
标识
DOI:10.1002/advs.202401855
摘要
Abstract Clinically, chronic pain and depression often coexist in multiple diseases and reciprocally reinforce each other, which greatly escalates the difficulty of treatment. The neural circuit mechanism underlying the chronic pain/depression comorbidity remains unclear. The present study reports that two distinct subregions in the paraventricular thalamus (PVT) play different roles in this pathological process. In the first subregion PVT posterior (PVP), glutamatergic neurons (PVP Glu ) send signals to GABAergic neurons (VLPAG GABA ) in the ventrolateral periaqueductal gray (VLPAG), which mediates painful behavior in comorbidity. Meanwhile, in another subregion PVT anterior (PVA), glutamatergic neurons (PVA Glu ) send signals to the nucleus accumbens D1‐positive neurons and D2‐positive neurons (NAc D1→D2 ), which is involved in depression‐like behavior in comorbidity. This study demonstrates that the distinct thalamo‐subcortical circuits PVP Glu →VLPAG GABA and PVA Glu →NAc D1→D2 mediated painful behavior and depression‐like behavior following spared nerve injury (SNI), respectively, which provides the circuit‐based potential targets for preventing and treating comorbidity.
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