| Literature DB >> 32841213 |
Jun-Bin Yin1,2,3,4, Shao-Hua Liang1,5, Fei Li1,6, Wen-Jun Zhao1,6, Yang Bai1,3, Yi Sun1,3,5, Zhen-Yu Wu1,3, Tan Ding7, Yan Sun6, Hai-Xia Liu1, Ya-Cheng Lu1, Ting Zhang1, Jing Huang1, Tao Chen1, Hui Li1,3, Zhou-Feng Chen3, Jing Cao8, Rui Ren4, Ya-Nan Peng4, Juan Yang4, Wei-Dong Zang8, Xiang Li9, Yu-Lin Dong1, Yun-Qing Li1,4,8.
Abstract
The dorsal medial prefrontal cortex (dmPFC) has been recognized as a key cortical area for nociceptive modulation. However, the underlying neural pathway and the function of specific cell types remain largely unclear. Here, we show that lesions in the dmPFC induced an algesic and anxious state. Using multiple tracing methods including a rabies-based transsynaptic tracing method, we outlined an excitatory descending neural pathway from the dmPFC to the ventrolateral periaqueductal gray (vlPAG). Specific activation of the dmPFC/vlPAG neural pathway by optogenetic manipulation produced analgesic and antianxiety effects in a mouse model of chronic pain. Inhibitory neurons in the dmPFC were specifically activated using a chemogenetic approach, which logically produced an algesic and anxious state under both normal and chronic pain conditions. Antagonists of the GABAA receptor (GABAAR) or mGluR1 were applied to the dmPFC, which produced analgesic and antianxiety effects. In summary, the results of our study suggest that the dmPFC/vlPAG neural pathway might participate in the maintenance of pain thresholds and antianxiety behaviors under normal conditions, while silencing or suppressing the dmPFC/vlPAG pathway might be involved in the initial stages and maintenance of chronic pain and the emergence of anxiety-like behaviors.Entities:
Keywords: Depression; Neuroscience; Pain
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Year: 2020 PMID: 32841213 PMCID: PMC7685740 DOI: 10.1172/JCI127607
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 19.456