Reduction of voltage-dependent currents by ethanol contributes to inhibition of NMDA receptor-mediated excitatory synaptic transmission.
Previous studies have shown inhibitory effects of EtOH on NMDA receptor-mediated synaptic transmission in several brain regions. We examined this effect of EtOH under both current clamp and voltage clamp conditions in the basolateral amygdala because of the putative role of the amygdala in mediating anxiolytic effects of EtOH. We found that EtOH reduced NMDA receptor-mediated synaptic responses. In addition, we found that NMDA receptor-mediated depolarizations could also activate a voltage-dependent regenerative potential which was also sensitive to EtOH. Pharmacological characterization of this current was consistent with a high-threshold Ca2+ current. This current also exhibited a pronounced tendency towards transient enhancement upon withdrawal of EtOH.
Calton, JL; Wilson, WA; Moore, SD
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