Neurocircuit of chronic pain and pain-induced negative emotions and regulatory mechanisms of electroacupuncture
Neurocircuit of chronic pain and pain-induced negative emotions and regulatory mechanisms of electroacupuncture
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DOI：
10.1016/j.wjam.2022.09.003
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Man LI
中科院分区：
文献类型：
--
作者：
Zi-yue ZHANG;Wen-xin ZHONG;Kai-ling ZHANG;Man LI
Chronic pain is a common clinical condition that is frequently linked to negative emotions such as anxiety and depression. Electroacupuncture (EA) has been shown to have beneficial therapeutic effects in analgesia and the reduction of pain-induced negative emotions, and promising results have been obtained in the study of its neural circuit mechanism. Optogenetics, chemogenetics, neurocircuit tracing, functional magnetic resonance imaging (fMRI), and conditional gene knockdown experiments have shown that EA activates parvalbumin (PV) interneurons in the anterior cingulate cortex (ACC), inhibits Protein kinase Mzeta-glutamate receptor (PKMzeta-GluR1) signaling pathway in ACC, and upregulates the expression of the neuropeptide S/neuropeptide S receptor (NPS/NPSR) system in ACC to alleviate pain and pain-induced anxiety. EA activates endogenous cannabinoid receptors 1(CB1Rs), inhibits γ-aminobutyric acid (GABA)-ergic neurons and activates glutamatergic neurons in the ventrolateral periaqueductal gray (vlPAG) to exert an analgesic effect, while EA exerts an anxiolytic effect by downregulating CB1R in GABAergic neurons in the ventral hippocampus (vHPC). EA relieves only pain-induced anxiety but not pain through inhibiting the rostral anterior cingulate cortex (rACC) Glu -thalamus circuit. By inhibiting the medial prefrontal cortex (mPFC) Glu -vlPAG GABA circuit, EA relieves only pain but not pain-induced anxiety. EA activated dopamine receptor D1 (DRD1) or inhibited dopamine receptor D2 (DRD2) in the basolateral amygdala (BLA) to alleviate anxiety-like behaviors. Taken together, these findings would offer a novel theoretical framework for a thorough investigation of theoretical studies and clinical promotion of EA analgesic mechanisms.
