Acute effects of ethanol on glutamate receptors

Basic Clin Pharmacol Toxicol. 2012 Jul;111(1):4-13. doi: 10.1111/j.1742-7843.2012.00879.x. Epub 2012 Apr 21.

Abstract

Several studies have revealed that acute ethanol inhibits the function of glutamate receptors. Glutamate receptor-mediated synaptic plasticity, such as N-methyl-D-aspartate-dependent long-term potentiation, is also inhibited by ethanol. However, the inhibition seems to be restricted to certain brain areas such as the hippocampus, amygdala and striatum. Ethanol inhibition of glutamate receptors generally requires relatively high concentrations and may therefore explain consequences of severe ethanol intoxication such as impairment of motor performance and memory. Effects of ethanol on glutamate system of developing nervous system may have a role in causing foetal alcohol syndrome. Newly found regulatory proteins of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid AMPA receptors seem to affect ethanol inhibition thus opening new lines of research.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amygdala / drug effects
  • Amygdala / metabolism
  • Animals
  • Ethanol / toxicity*
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Humans
  • Long-Term Potentiation / drug effects
  • N-Methylaspartate / antagonists & inhibitors
  • N-Methylaspartate / drug effects
  • N-Methylaspartate / metabolism
  • Neuronal Plasticity / drug effects
  • Receptors, AMPA / antagonists & inhibitors
  • Receptors, AMPA / drug effects
  • Receptors, AMPA / metabolism
  • Receptors, Glutamate / drug effects*
  • Receptors, Glutamate / metabolism*
  • Receptors, Kainic Acid / antagonists & inhibitors
  • Receptors, Kainic Acid / drug effects
  • Toxicity Tests, Acute

Substances

  • Receptors, AMPA
  • Receptors, Glutamate
  • Receptors, Kainic Acid
  • Ethanol
  • N-Methylaspartate