Actions of ethanol on gamma-aminobutyric acid-activated chloride channels.
Ethanol appears to exert its intoxicating effects, at least partly, by potentiating gamma-aminobutyric acid (GABA) mediated inhibitory synaptic transmission in the brain. Work over the past decade using mouse lines selected for different ethanol sensitivities has implicated GABA-activated chloride channels as a potential target of ethanol. More recently, molecular biological techniques have identified a subunit (gamma 2L) of the GABA channel which appears to be required for the effects of ethanol on GABA channels. The presence of this subunit, however, cannot account for the full degree of potentiation of GABA responses observed in native GABA channels. Ongoing research is directed at identifying other factors which might be involved in the effects of ethanol on GABA channels and in understanding ethanol's molecular mechanism of action. Such information could be vital for designing drugs to combat ethanol intoxication.
Weiss
D S
DS
Department of Physiology and Biophysics, University of South Florida College of Medicine.
D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D000431:Ethanol / Q000494:pharmacology*; D015640:Ion Channel Gating / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects*; D051379:Mice; D011963:Receptors, GABA-A / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D002712:Chlorides; D007473:Ion Channels; D011963:Receptors, GABA-A; D000431:Ethanol; D005680:gamma-Aminobutyric Acid