Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states

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

Research output: Contribution to journalArticlepeer-review

62 Scopus citations


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.

Original languageEnglish
Pages (from-to)542-553
Number of pages12
JournalNature Neuroscience
Issue number4
StatePublished - Apr 2021
Externally publishedYes


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