Alcohol intoxication: ion channels and genetics.
Acute in vitro exposure to ethanol and other intoxicant-anesthetics activates gamma-aminobutyric acid (GABA)-stimulated chloride channels and inhibits voltage-dependent calcium and sodium channels of isolated brain membranes. The question of whether these neurochemical actions are responsible for intoxication in vivo has been addressed using animal populations displaying genetic differences in sensitivity to alcohol and benzodiazepine intoxication. These genetic approaches include inbred strains, selected lines, recombinant inbred strains, and heterogeneous stocks. Genetic differences in ion channel function provide strong evidence for a role of the GABA-stimulated chloride channel in ethanol and benzodiazepine intoxication; the role of calcium and sodium channels is less clear.
Harris
R A
RA
Denver Veterans Administration Medical Center, Colorado.
Allan
A M
AM
D000435:Alcoholic Intoxication / Q000235:genetics* / Q000503:physiopathology; D000818:Animals; D018118:Chloride Channels; D002712:Chlorides / Q000502:physiology; D004594:Electrophysiology; D007473:Ion Channels / Q000502:physiology*; D008565:Membrane Proteins / Q000502:physiology; D051379:Mice; D008815:Mice, Inbred Strains; D015221:Potassium Channels / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D018118:Chloride Channels; D002712:Chlorides; D007473:Ion Channels; D008565:Membrane Proteins; D015221:Potassium Channels; D005680:gamma-Aminobutyric Acid