Low-frequency electro-acupuncture reduces the nociceptive response and the pain mediator enhancement induced by nerve growth factor

Neurosci Lett. 2009 Jan 16;449(3):173-7. doi: 10.1016/j.neulet.2008.11.003. Epub 2008 Nov 7.

Abstract

A number of studies have shown that the potential clinical benefits of nerve growth factor (NGF) administration are limited by its hyperalgesic side effects. The ancient therapeutic technique of acupuncture and its modern derivate electro-acupuncture (EA) have been proven effective in reducing hyperalgesia as well as nociceptive and neuropathic pain in several pathological conditions. The present study addresses the question of whether EA can influence the hyperalgesia induced by NGF administration. We treated adult healthy rats with repeated injections of murine NGF and/or low-frequency electro-acupuncture. We found that EA was able to counteract the NGF-induced hyperalgesic response when assessed by a hot plate test. Moreover, EA counteracted the NGF-driven variation of substance P (SP) and transient receptor potential vanilloid type 1 (TRPV1) response in both hind-paw skin as well as the corresponding dorsal root ganglia (DRG). Our findings indicate that low-frequency EA could be useful as a supportive therapy to reduce NGF-induced side effects, such as hypersensitivity and hyperalgesia, when clinical treatment with NGF is necessary.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Electroacupuncture / methods*
  • Enzyme-Linked Immunosorbent Assay
  • Ganglia, Spinal / metabolism
  • Gene Expression Regulation / drug effects*
  • Hyperalgesia / chemically induced*
  • Hyperalgesia / therapy*
  • Male
  • Mice
  • Nerve Growth Factor* / blood
  • Pain Measurement
  • Pain Threshold / drug effects
  • Pain Threshold / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Reaction Time / drug effects
  • Skin / innervation
  • Skin / metabolism
  • Substance P / metabolism
  • TRPV Cation Channels / metabolism

Substances

  • TRPV Cation Channels
  • Trpv1 protein, rat
  • Substance P
  • Nerve Growth Factor