Glutamate antagonists prevent morphine withdrawal in mice and guinea pigs

Neurosci Lett. 1991 Jan 28;122(2):270-2. doi: 10.1016/0304-3940(91)90875-t.

Abstract

The effects of excitatory amino acid antagonists on increased cortical acetylcholine release and behavioral hyperactivity induced by naloxone in morphine tolerant guinea pigs and mice were studied. The results show that the N-methyl-D-aspartic acid (NMDA) antagonist MK-801 (0.1-1 mg/kg, i.p.) injected 30 min before naloxone (3 mg/kg, s.c.) dose-dependently prevented the neurochemical and behavioral signs of morphine withdrawal in guinea pigs and mice. The non-selective antagonist glutamic acid diethylester only at 100 mg/kg i.p. reduced the naloxone-induced increase of cortical acetylcholine release without affecting the behavioral changes. These findings indicate that the activation of excitatory amino acid receptors, mainly the NMDA receptors, plays a relevant role in the expression of opiate abstinence.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / metabolism
  • Animals
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism*
  • Dizocilpine Maleate / pharmacology
  • Drug Implants
  • Drug Tolerance*
  • Excitatory Amino Acid Antagonists*
  • Glutamates / pharmacology*
  • Guinea Pigs
  • Kinetics
  • Mice
  • Morphine / administration & dosage
  • Morphine / toxicity*
  • N-Methylaspartate / antagonists & inhibitors
  • Naloxone / pharmacology*
  • Parietal Lobe / drug effects
  • Parietal Lobe / metabolism
  • Psychotropic Drugs / pharmacology*
  • Substance Withdrawal Syndrome / prevention & control*

Substances

  • Drug Implants
  • Excitatory Amino Acid Antagonists
  • Glutamates
  • Psychotropic Drugs
  • glutamic acid diethyl ester
  • Naloxone
  • N-Methylaspartate
  • Dizocilpine Maleate
  • Morphine
  • Acetylcholine