An early study in rats [58] found that EtOH reduces the duration of epileptiform activity and NMDA-mediated synaptic responses in BLA neurons. At 50mM, EtOH produces a 40% reduction in the duration of epileptiform activity, while 20mM EtOH decreases this response by 20%. Calton and colleagues [59] later reported that EtOH inhibits NMDA-mediated currents in the rat BLA at medium but not low concentrations. Specifically, these authors found that 44 mM EtOH reduces the amplitude of NMDA receptor-mediated EPSCs by ~30%; no effect of EtOH on NMDA currents was detected at 11 or 22 mM EtOH. These authors later confirmed that EtOH reduces NMDA receptor-mediated synaptic responses in the BLA, and further found that NMDA receptor-mediated depolarizations activate a voltage-dependent regenerative potential that is also reduced by EtOH [60]. In this set of experiments, 44mM EtOH reduced the amplitude of NMDA receptor-mediated EPSPs by up to 30%. The same EtOH concentration significantly reduced spike area and increased the stimulus threshold for spike activation. Finally, these authors report that 44mM EtOH reduces inward currents in BLA pyramidal neurons without shifting the current/voltage relationship of these currents; specifically, EtOH inhibited the steady-state current by ~ 25%.
