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Open Access Research article

Electroacupuncture activates corticotrophin-releasing hormone-containing neurons in the paraventricular nucleus of the hypothalammus to alleviate edema in a rat model of inflammation

Aihui Li1, Lixing Lao1, Yi Wang2, Jiajia Xin1, Ke Ren3, Brian M Berman1, Ming Tan4 and Ruixin Zhang1*

Author Affiliations

1 Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, MD 21201, USA

2 Shanghai University of Traditional Chinese Medicine, Yueyang Affiliated Hospital, Shanghai, China

3 Dept. of Biomedical Sciences, Dental School, University of Maryland, Baltimore, MD 21201, USA

4 Division of Biostatistics, University of Maryland Greenebaum Cancer Center, Baltimore, MD 21201, USA

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BMC Complementary and Alternative Medicine 2008, 8:20  doi:10.1186/1472-6882-8-20

Published: 12 May 2008

Abstract

Background

Studies show that electroacupuncture (EA) has beneficial effects in patients with inflammatory diseases. This study investigated the mechanisms of EA anti-inflammation, using a rat model of complete Freund's adjuvant (CFA)-induced hind paw inflammation and hyperalgesia.

Design

Four experiments were conducted on male Sprague-Dawley rats (n = 6–7/per group). Inflammation was induced by injecting CFA into the plantar surface of one hind paw. Experiment 1 examined whether EA increases plasma adrenocorticotropic hormone (ACTH) levels. Experiments 2 and 3 studied the effects of the ACTH and corticotropin-releasing hormone (CRH) receptor antagonists, ACTH(11–24) and astressin, on the EA anti-edema. Experiment 4 determined whether EA activates CRH neurons in the paraventricular nucleus of the hypothalammus. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice for 20 min each, once immediately post and again 2 hr post-CFA. Plasma ACTH levels, paw thickness, and paw withdrawal latency to a noxious thermal stimulus were measured 2 h and 5 h after the CFA.

Results

EA significantly increased ACTH levels 5 h (2 folds) after CFA compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in ACTH. ACTH(11–24) and astressin blocked EA anti-edema but not EA anti-hyperalgesia. EA induced phosphorylation of NR1, an essential subunit of the N-methyl-D-aspartic acid (NMDA) receptor, in CRH-containing neurons of the paraventricular nucleus.

Conclusion

The data demonstrate that EA activates CRH neurons to significantly increase plasma ACTH levels and suppress edema through CRH and ACTH receptors in a rat model of inflammation.