Ethanol and the gamma-aminobutyric acid-benzodiazepine receptor complex

J Neurochem. 1984 Apr;42(4):1062-8. doi: 10.1111/j.1471-4159.1984.tb12711.x.


Ethanol appears to enhance gamma-aminobutyric acid (GABA)-mediated synaptic transmission. Using radioligand binding techniques, we investigated the possibility that the GABA-benzodiazepine receptor complex is the site responsible for this effect. Ethanol at concentrations up to 100 mM failed to alter binding of [3H]flunitrazepam (FNZ), [3H]Ro 15-1788, or [3H]methyl-beta-carboline-3-carboxylate (MBCC) to benzodiazepine receptors, or of [3H]muscimol to GABA receptors in rat brain membranes. Scatchard analyses of the binding of these radioligands at 4 degrees C and 37 degrees C revealed no significant effects of 100 mM ethanol on receptor affinity or number. A variety of drugs as well as chloride ion increased binding of [3H]FNZ and/or [3H]muscimol, but these influences were not modified by ethanol. These findings indicate that ethanol probably potentiates GABAergic neurotransmission at a signal transduction site beyond the GABA-benzodiazepine receptor complex.

Publication types

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

MeSH terms

  • Animals
  • Benzodiazepinones / metabolism
  • Brain / metabolism*
  • Carbolines / metabolism
  • Ethanol / pharmacology*
  • Flumazenil
  • Flunitrazepam / metabolism
  • Male
  • Membranes / metabolism
  • Muscimol / metabolism
  • Rats
  • Rats, Inbred Strains
  • Receptors, Cell Surface / metabolism*
  • Receptors, GABA-A
  • Temperature
  • gamma-Aminobutyric Acid / metabolism*


  • Benzodiazepinones
  • Carbolines
  • Receptors, Cell Surface
  • Receptors, GABA-A
  • 1-methyl-beta-carboline-3-carboxylic acid
  • Muscimol
  • Ethanol
  • Flumazenil
  • gamma-Aminobutyric Acid
  • Flunitrazepam