The study investigates the inhibitory effects of ethanol (EtOH) on NMDA-activated ion currents in voltage-clamped hippocampal neurons. Ethanol significantly reduced the amplitude of the NMDA-activated current, with a 61% reduction observed at 50 mM EtOH. This inhibition was concentration-dependent and was more potent than the effects on kainate and quisqualate-activated currents. The potency of various alcohols to inhibit NMDA-activated currents was linearly related to their intoxicating potencies, suggesting that alcohol-induced inhibition of NMDA receptor activation may contribute to neural and cognitive impairments associated with intoxication. The mechanism of this inhibition is unclear but may involve changes in membrane fluidity or interactions with the NMDA receptor-ionophore complex.The study investigates the inhibitory effects of ethanol (EtOH) on NMDA-activated ion currents in voltage-clamped hippocampal neurons. Ethanol significantly reduced the amplitude of the NMDA-activated current, with a 61% reduction observed at 50 mM EtOH. This inhibition was concentration-dependent and was more potent than the effects on kainate and quisqualate-activated currents. The potency of various alcohols to inhibit NMDA-activated currents was linearly related to their intoxicating potencies, suggesting that alcohol-induced inhibition of NMDA receptor activation may contribute to neural and cognitive impairments associated with intoxication. The mechanism of this inhibition is unclear but may involve changes in membrane fluidity or interactions with the NMDA receptor-ionophore complex.