Phorbol ester blocks the increase of a high affinity GTPase activity induced by delta 2-opioid receptor agonist in the mouse spinal cord

Eur J Pharmacol. 1996 Aug 29;310(2-3):R1-3. doi: 10.1016/0014-2999(96)00493-1.

Abstract

The high affinity GTPase activity in the mouse spinal cord was increased in a concentration-dependent manner by a selective delta 2-opioid receptor agonist, [D-Ala2]deltorphin II (0.1-1 microM). This increase of GTPase activity induced by [D-Ala2]deltorphin II was completely blocked by co-incubation with a selective delta 2-opioid receptor antagonist, naltriben (0.1 microM). A protein kinase C activator, phorbol 12,13-dibutyrate (PDB; 0.1-10 microM), which given alone had no effect on basal GTPase activity, blocked dose-dependently the increase of GTPase activity induced by [D-Ala2]deltorphin II (1 microM). Our results indicate the possibility that activation of protein kinase C by phorbol ester uncouples the delta 2-opioid receptor from G-proteins in the spinal cord.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Enzyme Activation
  • GTP Phosphohydrolases / metabolism*
  • Male
  • Mice
  • Mice, Inbred ICR
  • Oligopeptides / pharmacology*
  • Phorbol 12,13-Dibutyrate / pharmacology*
  • Receptors, Opioid, delta / agonists*
  • Spinal Cord / drug effects*
  • Spinal Cord / enzymology

Substances

  • Oligopeptides
  • Receptors, Opioid, delta
  • deltorphin II, Ala(2)-
  • Phorbol 12,13-Dibutyrate
  • GTP Phosphohydrolases