Ethanol Inhibition of AMPA and Kainate Receptor-Mediated Depolarizations of Hippocampal Area CA1

摘要: Longitudinal hippocampal slices were prepared from adult female rats. The excitatory amino acids, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) and kainic acid, applied to area CA1, the resulting depolarizations measured using grease-gap electrophysiological technique. Agonist dose-response curves generated in presence absence of various concentrations ethanol. Ethanol (25-200 mM) significantly attenuated that produced by each agonist. In addition, we found ethanol potently antagonized kainate-induced across agonist concentration-response curve, whereas it suppressed only AMPA responses induced with moderate-to-high concentrations. These results indicate has potent antagonist actions against non-N-methyl-D-aspartate (NMDA) acid-induced neuronal CA1. Moreover, relative potency depends on specific tested concentration This suggests that, addition known effects NMDA receptor-mediated activity, may also attenuate ongoing "fast" glutamatergic synaptic activity hippocampus.