Ethanol inhibits excitotoxicity in cerebral cortical cultures.
Excitatory amino acid neurotransmitters have been implicated in the pathogenesis of cerebral ischemia and related forms of acute neuronal injury. Because ethanol inhibits cellular signaling mechanisms activated by excitatory amino acids, we examined its effect on excitatory amino acid-induced toxicity in neuron-enriched cultures prepared from rat cerebral cortex. Both glutamate and N-methyl-D-aspartate (NMDA) were toxic to cultured cortical cells, as demonstrated by a reduction in their ability to exclude trypan blue dye, and this toxicity was reversed by the NMDA antagonist MK-801. Ethanol (100 mM) provided partial protection from the excitotoxic effect of NMDA. Thus ethanol, like conventional excitatory amino acid antagonists, can attenuate excitotoxic neuronal injury in vitro.
Lustig
H S
HS
Department of Neurology, University of California, San Francisco 94110.
Chan
J
J
Greenberg
D A
DA
D000818:Animals; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects*; D016291:Dizocilpine Maleate / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D016202:N-Methylaspartate / Q000494:pharmacology / Q000633:toxicity; D009474:Neurons / Q000187:drug effects; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains
D000431:Ethanol; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate