Role of gap junction in the expression of morphine-induced antinociception

Eur J Pharmacol. 2006 Mar 27;535(1-3):169-71. doi: 10.1016/j.ejphar.2006.01.038. Epub 2006 Mar 7.

Abstract

The present study was undertaken to investigate whether gap junctional communication could be involved in morphine-induced antinociceptive response using blockers of the gap junctional channel, carbenoxolone and Gap27. Intrathecal pretreatment with either carbenoxolone or Gap27 caused a dose-dependent attenuation of morphine-induced antinociception. Furthermore, the dose-response line for morphine-induced antinociception was shifted to the right by 2.53-fold following intrathecal treatment with carbenoxolone. These findings suggest that gap-junctional-dependent communication in the mouse spinal cord may play, at least in part, a role in the expression of morphine-induced antinociception.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analgesics, Opioid / administration & dosage
  • Analgesics, Opioid / pharmacology*
  • Animals
  • Carbenoxolone / administration & dosage
  • Carbenoxolone / pharmacology
  • Connexins / administration & dosage
  • Connexins / pharmacology
  • Dose-Response Relationship, Drug
  • Gap Junctions / physiology*
  • Injections, Spinal
  • Injections, Subcutaneous
  • Male
  • Mice
  • Mice, Inbred ICR
  • Morphine / administration & dosage
  • Morphine / pharmacology*
  • Oligopeptides
  • Pain / prevention & control*
  • Pain Measurement / methods

Substances

  • Analgesics, Opioid
  • Connexins
  • Oligopeptides
  • gap 27 peptide
  • Morphine
  • Carbenoxolone