Involvement of neuronal chloride channels in ethanol intoxication, tolerance, and dependence.
Studies of the role of neuronal chloride channels in ethanol action have focused on chloride channels coupled to gamma-aminobutyric acid (GABA) receptors. Ethanol intoxication is hypothesized to result from enhancement of GABA action, leading to increased chloride conductance and decreased neuronal excitability. Chronic ethanol treatment is suggested to produce a subsensitivity to GABA, leading to decreased action of ethanol and hyperexcitability on withdrawal of ethanol. Behavioral, electrophysiological, and biochemical studies of acute and chronic ethanol treatments on the GABA-regulated chloride channels of brain are reviewed.
D000435:Alcoholic Intoxication / Q000378:metabolism*; D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D011963:Receptors, GABA-A / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D002712:Chlorides; D007473:Ion Channels; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid