The same study also concluded that ethanol significantly diminished NMDA receptor-mediated excitatory postsynaptic currents in both species [33]. Others have also found a link between ethanol and disruption in hippocampal NMDA receptor-mediated signaling using bath application of 50mM ethanol to hippocampal slice preparations. One group found that 50mM ethanol application decreased the frequency of NMDA-R miniature excitatory postsynaptic currents (mEPSCs) and inhibited depolarization-induced potentiation in CA1 hippocampal neurons [34, 35]. More recent work found that application of 40mM ethanol decreased AMPA receptor-and NMDA receptor-mediated field excitatory postsynaptic potentials (fEPSPs) [36]. Kainate receptors (another subtype of glutamate-gated ionotropic receptors) have also been implicated and are critical in the excitation of CA1 hippocampal interneurons. Recordings of spontaneous IPSCs from rat hippocampal slices upon application of 20–40mM ethanol demonstrated inhibited interneuron action potential firing, via a significant inhibition of kainate receptors [37]. Lower ethanol concentrations appear to modulate glutamatergic signaling within the hippocampus as well and may have various molecular targets depending on cell type or region involved. Importantly, 30–40mM concentrations of ethanol are likely ideal for studying physiologically relevant hippocampal mechanisms of
