The neuroanatomical specificity of ethanol action on ligand-gated ion channels: a hypothesis

G R Breese; A L Morrow; P E Simson; H E Criswell; T J McCown; G E Duncan; W J Keir

The neuroanatomical specificity of ethanol action on ligand-gated ion channels: a hypothesis

Alcohol Alcohol Suppl. 1993:2:309-13.

Authors

G R Breese¹, A L Morrow, P E Simson, H E Criswell, T J McCown, G E Duncan, W J Keir

Affiliation

¹ Brain and Development Research Center, University of North Carolina at Chapel Hill 27599, USA.

PMID: 7538301

Abstract

The studies described will demonstrate that the subunit composition of a GABAA receptor allows ethanol to enhance responses to GABA. Since we have determined that ethanol will influence responses to glycine, nicotine and NMDA in some, but not all, neurons with receptors to these agonists, we hypothesize that specific receptor subtypes of these ligand-gated ion channels will be affected by ethanol.

Publication types

Review

MeSH terms

Animals
Brain / anatomy & histology
Brain / drug effects*
Brain / metabolism
Ethanol / toxicity*
Glycine / pharmacology
Humans
Ion Channels / drug effects*
Ion Channels / metabolism
Ligands
Models, Neurological
Muscimol / pharmacology
N-Methylaspartate / pharmacology
Nicotine / pharmacology
Receptors, GABA-A / drug effects
Receptors, GABA-A / metabolism
gamma-Aminobutyric Acid / pharmacology

Substances

Ion Channels
Ligands
Receptors, GABA-A
Muscimol
Ethanol
gamma-Aminobutyric Acid
N-Methylaspartate
Nicotine
Glycine