Ethanol inhibits NMDA-activated current but does not alter GABA-activated current in an isolated adult mammalian neuron.
The effects of ethanol (EtOH) on membrane ion currents activated by N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA) were studied under voltage-clamp conditions in isolated sensory neurons within hours of being dissociated from adult rats. The amplitude of the ion current activated by NMDA was decreased in the presence of 2.5-100 mM EtOH (IC50, 10 mM or 0.05% EtOH), a concentration range that produces intoxication. The amplitude of the GABA-activated Cl- current, on the other hand, was not significantly affected by this concentration range of EtOH. The observations suggest that some of the neural and cognitive impairments associated with EtOH intoxication may result from inhibition of the NMDA-activated ion current.
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Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852.
Lovinger
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D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D016202:N-Methylaspartate; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D001224:Aspartic Acid; D000431:Ethanol; D005680:gamma-Aminobutyric Acid; D016202:N-Methylaspartate