Ethanol potentiates GABA- and glycine-induced chloride currents in chick spinal cord neurons

Brain Res. 1988 Jul 12;455(2):377-80. doi: 10.1016/0006-8993(88)90098-4.

Abstract

The effects of acute ethanol exposure of chick spinal cord neurons were studied in tissue culture, using whole-cell voltage-clamp techniques. Results indicate that ethanol produces a persistent increase in the sensitivity of spinal neurons to GABA and glycine, with no change in input resistance or resting membrane potential. Glutamate responses, in contrast, are unaffected by ethanol.

Publication types

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

MeSH terms

  • Animals
  • Azides / pharmacology
  • Benzodiazepines / pharmacology
  • Cells, Cultured
  • Chick Embryo
  • Chlorides / physiology*
  • Ethanol / pharmacology*
  • Glutamates / pharmacology
  • Glutamic Acid
  • Glycine / pharmacology*
  • Membrane Potentials / drug effects
  • Receptors, GABA-A / drug effects
  • Receptors, GABA-A / physiology
  • Receptors, Glycine
  • Receptors, Neurotransmitter / drug effects
  • Receptors, Neurotransmitter / physiology
  • Spinal Cord / cytology
  • Spinal Cord / drug effects
  • Spinal Cord / physiology*
  • gamma-Aminobutyric Acid / pharmacology*

Substances

  • Azides
  • Chlorides
  • Glutamates
  • Receptors, GABA-A
  • Receptors, Glycine
  • Receptors, Neurotransmitter
  • Benzodiazepines
  • Ethanol
  • Glutamic Acid
  • gamma-Aminobutyric Acid
  • Ro 15-4513
  • Glycine