Magnesium-dependent inhibition of N-methyl-D-aspartate receptor-mediated synaptic transmission by ethanol.
Previous studies have indicated that ethanol (EtOH) has a relatively specific effect on excitatory synaptic transmission by inhibiting function of the N-methyl-D-aspartate receptor. We have found that EtOH potently inhibits N-methyl-D-aspartate-mediated synaptic currents in the basolateral amygdala, a brain region associated with actions of anxiolytic agents such as EtOH. This inhibitory effect of EtOH requires the presence of magnesium (Mg++). The dependence of the effect of EtOH on the presence of Mg++ suggests a possible molecular site of the action of EtOH in the vicinity of Mg++ binding sites on the N-methyl-D-aspartate receptor-channel complex. Because EtOH consumption may result in reductions in free brain Mg++, this dynamic interaction between EtOH and Mg++ may have important implications for understanding the behavioral effects of EtOH.
Calton
J L
JL
Department of Psychiatry, Duke University Medical Center, Durham, North Carolina, USA.
Wilson
W A
WA
Moore
S D
SD
D000679:Amygdala / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D004357:Drug Synergism; D000431:Ethanol / Q000494:pharmacology*; D018698:Glutamic Acid; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*; D009435:Synaptic Transmission / Q000187:drug effects*
D002492:Central Nervous System Depressants; D016194:Receptors, N-Methyl-D-Aspartate; D000431:Ethanol; D018698:Glutamic Acid; D008274:Magnesium