Transgene-mediated enkephalin expression attenuates signs of naloxone-precipitated morphine withdrawal in rats with neuropathic pain

Shuanglin Hao, Jian Hu, David J. Fink

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Chronic morphine exposure induces physical dependence and tolerance. Previous studies have shown that there is a decrease in met-enkephalin levels in states of morphine physical dependence, and that increasing enkephalin during opiate physical withdrawal ameliorates the severity of the morphine withdrawal syndrome. In order to investigate the role of spinal opioid peptide in the phenomenon of naloxone-precipitated withdrawal we examined the effect of herpes simplex virus vector-mediated overexpression of proenkephalin in lumbar dorsal root ganglia in rats with neuropathic pain treated with morphine. The morphine physical dependence was induced by chronic administration of intraperitoneal (IP) morphine for 2 weeks. Rats with neuropathic pain inoculated subcutaneously with the vector-mediated overexpression of proenkephalin showed a significant reduction in jumps, 'wet-dog' shakes, diarrhea and ptosis precipitated by naloxone after 2 weeks of morphine treatment. The global withdrawal score was also reduced significantly by vector-mediated overexpression of proenkephalin. These studies demonstrate a role for opioid peptide in the spinal cord in mediating some of the withdrawal response.

Original languageEnglish (US)
Pages (from-to)84-89
Number of pages6
JournalBehavioural Brain Research
Volume197
Issue number1
DOIs
StatePublished - Jan 30 2009
Externally publishedYes

Keywords

  • Enkephalin
  • Gene therapy
  • Herpes simplex
  • Morphine
  • Physical withdrawal

ASJC Scopus subject areas

  • Behavioral Neuroscience

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