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Neural Plasticity
Volume 2016 (2016), Article ID 1437148, 14 pages
Research Article

Electroacupuncture Treatment Alleviates Central Poststroke Pain by Inhibiting Brain Neuronal Apoptosis and Aberrant Astrocyte Activation

1Key Laboratory of Chinese Internal Medicine of MOE, Beijing Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
2Department of Tuina and Pain, Beijing Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
3Chinese Evidence-Based Medicine Center, West China Hospital, Sichuan University, Sichuan 610041, China
4Department of Pharmacology, School of Pharmaceutical Sciences, South-Central University for Nationalities, No. 182, Minyuan Road, Wuhan 430074, China

Received 20 July 2016; Revised 30 August 2016; Accepted 1 September 2016

Academic Editor: Jian Kong

Copyright © 2016 Gui-Hua Tian et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.