NMDARs are involved in acute ethanol intoxication and addiction-related behaviors (Krystal et al., 2003; Möykkynen and Korpi, 2012). At intoxicating concentrations ethanol causes an inhibition of NMDARs (Lovinger et al., 1990; Proctor et al., 2006; Xu and Woodward, 2006). The role of NMDARs in γ oscillations is debated. NMDARs are not necessary for the phasic synaptic excitation in γ-generating networks (Fisahn et al., 2004), which is in line with our observation that D-AP5 itself had no effect on control γ oscillation. However, NMDAR blockade enhances the ethanol-induced suppression of γ, which may be associated with the contribution of NMDAR to the tonic drive of interneurons (Middleton et al., 2008; Mann and Mody, 2010; Xue et al., 2011). The suppression of γ oscillations may reveal a critical dependence on the NMDAR-mediated drive of interneurons in the presence of ethanol. In line with our observations, a recent study showed that blocking the glycine(B) site of NMDRs potentiated ethanol intoxication (Debrouse et al., 2013).
