Electroacupuncture Treatment Alleviates Central Poststroke Pain by Inhibiting Brain Neuronal Apoptosis and Aberrant Astrocyte Activation. (27th September 2016)

• Record Type: Journal Article
• Authors: Tian, Gui-Hua; Tao, Shan-Shan; Chen, Man-Tang; Li, Yu-Sang; Li, You-Ping; Shang, Hong-Cai; Tang, Xiao-Yi; Chen, Jian-Xin; Tang, He-Bin
• Other Names: Kong Jian Academic Editor.
• Is Part Of: Neural plasticity. Volume 2016(2016)
• Publication Date: 2016-09-27
• Subjects: Neuroplasticity -- Periodicals; 612.82
• DOI: 10.1155/2016/1437148
• Languages: English
• ISSNs: 2090-5904

Abstract

Abstract : Electroacupuncture (EA) is reported to effectively relieve the central poststroke pain (CPSP). However, the underlying mechanism remains unclear. The present study investigated the detailed mechanisms of action of EA treatment at different frequencies for CPSP. A CPSP model was established with a single collagenase injection to the left ventral posterolateral nucleus of the thalamus. The EA-treated groups then received EA treatment at frequency of 2, 2/15, or 15 Hz for 30 min daily for five days. The pain-related behavioral responses, neuronal apoptosis, glial activation, and the expression of pain signal transmission-related factors ( β -catenin, COX-2, and NK-1R) were assessed using behavioral tests, Nissl staining, TUNEL staining, and immunohistochemical staining, respectively. The low-frequency EA treatment significantly (1) reduced brain tissue damage and hematoma sizes and (2) inhibited neuronal apoptosis, thereby exerting abirritative effects. Meanwhile, the high-frequency EA treatment induced a greater inhibition of the aberrant astrocyte activation, accompanied by the downregulation of the expressions of COX-2, β -catenin, and subsequently NK-1R, thereby alleviating inflammation and producing strong analgesic effects. Together, these findings suggest that CPSP is closely related to pathological changes of the neocortex and hippocampus. EA treatments at different frequencies may exert abirritative effects by inhibiting brain neuronal apoptosis and aberrant astrocyte activation in the brain.