• Yan Jin, Qian Meng, Lisheng Mei, Wenjie Zhou, Xia Zhu, Yu Mao, Wen Xie, Xulai Zhang, Min-Hua Luo, Wenjuan Tao, Haitao Wang, Jie Li, Juan Li, Xiangyao Li, and Zhi Zhang.
• Hefei National Laboratory for Physical Sciences at the Microscale, CAS Key laboratory of Brain Function and Disease, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei, PR China.
• Pain. 2020 Feb 1; 161 (2): 416-428.

AbstractChronic pain and anxiety symptoms are frequently encountered clinically, but the neural circuit mechanisms underlying the comorbid anxiety symptoms in pain (CASP) in context of chronic pain remain unclear. Using viral neuronal tracing in mice, we identified a previously unknown pathway whereby glutamatergic neurons from layer 5 of the hindlimb primary somatosensory cortex (S1) (Glu), a well-known brain region involved in pain processing, project to GABAergic neurons in the caudal dorsolateral striatum (GABA). In a persistent inflammatory pain model induced by complete Freund's adjuvant injection, enhanced excitation of the Glu→GABA pathway was found in mice exhibiting CASP. Reversing this pathway using chemogenetic or optogenetic approaches alleviated CASP. In addition, the optical activation of Glu terminals in the cDLS produced anxiety-like behaviors in naive mice. Overall, the current study demonstrates the putative importance of a novel Glu→GABA pathway in controlling at least some aspects of CASP.

35 keywords...

hide…