Acute ethanol increases the probability of GABA release in hippocampal CA1 pyramidal neurons and in the central nucleus of the amygdala (Wu et al., 2005; Li et al., 2014; Valenzuela and Jotty, 2015). Ethanol depresses the frequency, but not the amplitude of miniature excitatory post-synaptic currents (mEPSCs) in CA1 neurons, suggesting that ethanol reduces pyramidal cell excitability and thus phasic activation of interneurons (Badanich et al., 2013). However, previous study also reported that ethanol (25–75 mM) dose-dependently inhibits mEPSC amplitude and frequency, suggesting that the acute effects of ethanol on NMDAR signaling at hippocampal synapses are multifocal in nature (Hendricson et al., 2004).
