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Evidence-Based Complementary and Alternative Medicine
Volume 2011, Article ID 134545, 12 pages
Original Article

Electroacupuncture Zusanli (ST36) on Release of Nitric Oxide in the Gracile Nucleus and Improvement of Sensory Neuropathies in Zucker Diabetic Fatty Rats

Department of Obstetrics and Gynecology, David Geffen School of Medicine at University of California Los Angeles, Harbor-UCLA Medical Center, Torrance, CA 90502, USA

Received 23 April 2009; Accepted 8 July 2009

Copyright © 2011 Pei-Jing Rong and Sheng-Xing Ma. 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.


The purpose of these studies was to examine the effects of electroacupuncture (EA) Zusanli (ST36) on release of nitric oxide (NO) in the gracile nucleus (GN) and determine if functional neuropathic changes were modified by EA ST36-induced NO in the nucleus in Zucker diabetic fatty (ZDF) rats. The foot withdrawal responses to mechanical, thermal and cold stimuli were measured before and after EA stimulation. A microdialysis probe was implanted in the GN and dialysate samples were collected 20 min before, during and after EA ST36. Total nitrate and nitrite ( N O − 𝑥 ) concentrations in the samples were quantified by using chemiluminescence. The baseline dialysate N O − 𝑥 concentrations in the GN were decreased in ZDF rats compared to lean control (LC) rats ( 𝑃 < . 0 5 ). In ZDF rats, dialysate N O − 𝑥 releases in the GN were markedly increased during EA ST36, whereas in LC rats, the releases were moderately enhanced at 20–40 min after EA ST36. The withdrawal latencies to mechanical, cold and thermal stimuli were significantly improved 20 min after EA ST36 both in LC and ZDF rats, but not altered by non-acupoint stimulation. The withdrawal latencies to EA ST36 were further potentiated by 3-morpholinyl-sydnoneimine and inhibited by NG-Propyl-L-arginine infused into the GN in ZDF rats ( 𝑃 < . 0 5 ). These results show that EA ST36 increases NO release in the GN, and NO in the nucleus modifies withdrawal latencies to mechanical, cold, and thermal nociception stimuli. Data suggest that EA ST36 induces NO release in the GN, which contributes to improvement of sensory neuropathies in rats.