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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 848603, 7 pages
Research Article

Downregulation of Spinal G Protein-Coupled Kinase 2 Abolished the Antiallodynic Effect of Electroacupuncture

1Department of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, Institute of Acupuncture Research and Institutes of Brain Science, Collaborative Innovation Center for Brain Science, School of Basic Medical Science, Fudan University, Shanghai 200032, China
2Department of Pharmacology, School of Basic Medical Science, Fudan University, Shanghai 200032, China

Received 6 February 2015; Accepted 3 April 2015

Academic Editor: Gabino Garrido

Copyright © 2015 Huan Liu 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.


Acupuncture or electroacupuncture (EA) has been demonstrated to have a powerful antihypernociceptive effect on inflammatory pain. The attenuation of G protein-coupled receptor kinase 2 (GRK2) in spinal cord and peripheral nociceptor has been widely acknowledged to promote the transition from acute to chronic pain and to facilitate the nociceptive progress. This study was designed to investigate the possible role of spinal GRK2 in EA antiallodynic in a rat model with complete Freund’s adjuvant (CFA) induced inflammatory pain. EA was applied to ST36 (“Zusanli”) and BL60 (“Kunlun”) one day after CFA injection. Single EA treatment at day 1 after CFA injection remarkably alleviated CFA induced mechanical allodynia two hours after EA. Repeated EA displayed significant antiallodynic effect from 2nd EA treatment and a persistent effect was observed during the rest of treatments. However, downregulation of spinal GRK2 by intrathecal exposure of GRK2 antisense 30 mins after EA treatment completely eliminated both the transient and persistent antiallodynic effect by EA treatment. These pieces of data demonstrated that the spinal GRK2 played an important role in EA antiallodynia on inflammatory pain.