Impact Factor:

24.48

DOI number:

10.1038/s41593-021-00811-x

Journal:

Nature Neuroscience

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.

First Author:

Xia Zhu, Hao-Di Tang, Wan-Ying Dong, Fang Kang

Co-author:

An Liu, Yu Mao, Wen Xie, Xulai Zhang, Peng Cao, Wenjie Zhou, Haitao Wang, Zahra Farzinpour, Wenjuan Tao, Xiaoyuan Song, Yan Zhang, Tian Xue

Indexed by:

Journal paper

Correspondence Author:

Yan Jin, Juan Li, Zhi Zhang

Volume:

24

Issue:

4

Page Number:

542-553.

Translation or Not:

no

Date of Publication:

2021-04-01

Included Journals:

SCI

Links to published journals:

https://www.nature.com/articles/s41593-021-00811-x