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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 636848, 12 pages
Research Article

Attenuation of TRPV1 and TRPV4 Expression and Function in Mouse Inflammatory Pain Models Using Electroacupuncture

1Graduate Institute of Biotechnology, National Chung Hsing University, Taichung 40227, Taiwan
2Graduate Institute of Acupuncture Science, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan
3Acupuncture Research Center, China Medical University, Taichung 40402, Taiwan
4Graduate Institute of Integrated Medicine, China Medical University, Taichung 40402, Taiwan
5Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
6School of Chinese Medicine, China Medical University, Taichung 40402, Taiwan

Received 27 August 2012; Revised 15 October 2012; Accepted 18 October 2012

Academic Editor: Shao Li

Copyright © 2012 Wei-Hsin Chen 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.


Although pain is a major human affliction, our understanding of pain mechanisms is limited. TRPV1 (transient receptor potential vanilloid subtype 1) and TRPV4 are two crucial receptors involved in inflammatory pain, but their roles in EA- (electroacupuncture-) mediated analgesia are unknown. We injected mice with carrageenan (carra) or a complete Freund’s adjuvant (CFA) to model inflammatory pain and investigated the analgesic effect of EA using animal behavior tests, immunostaining, Western blotting, and a whole-cell recording technique. The inflammatory pain model mice developed both mechanical and thermal hyperalgesia. Notably, EA at the ST36 acupoint reversed these phenomena, indicating its curative effect in inflammatory pain. The protein levels of TRPV1 and TRPV4 in DRG (dorsal root ganglion) neurons were both increased at day 4 after the initiation of inflammatory pain and were attenuated by EA, as demonstrated by immunostaining and Western blot analysis. We verified DRG electrophysiological properties to confirm that EA ameliorated peripheral nerve hyperexcitation. Our results indicated that the AP (action potential) threshold, rise time, and fall time, and the percentage and amplitude of TRPV1 and TRPV4 were altered by EA, indicating that EA has an antinociceptive role in inflammatory pain. Our results demonstrate a novel role for EA in regulating TRPV1 and TRPV4 protein expression and nerve excitation in mouse inflammatory pain models.