Impact Factor:

8.8

DOI number:

10.1016/j.celrep.2019.11.003

Journal:

Cell Reports

Abstract:

While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeA/GluPF/S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeA/GluPF/S2 pathway in controlling at least some aspects of CP.

First Author:

Xia Zhu, Wenjie Zhou

Co-author:

Yan Jin, Haodi Tang, Peng Cao, Yu Mao, Wen Xie, Xulai Zhang, Fei Zhao, Min-Hua Luo, Haitao Wang, Jie Li, Wenjuan Tao, Zahra Farzinpour, Likui Wang, Xiangyao Li, Juan Li, Zheng-Quan Tang, Chenghua Zhou

Indexed by:

Journal paper

Correspondence Author:

Zhizhong Z Pan, Zhi Zhang

Volume:

29

Issue:

12

Page Number:

3847-3858.e5.

Translation or Not:

no

Date of Publication:

2019-12-17

Included Journals:

SCI

Links to published journals:

https://www.cell.com/cell-reports/fulltext/S2211-1247(19)31474-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124719314743%3Fshowall%3Dtrue