The suppression of γ oscillations by ethanol is likely to contribute to the behavioral effects associated with ethanol intoxication. Understanding the mechanisms underlying ethanol intoxication may provide cues for reversing it. Our observations imply that enhancing NMDAR could be a strategy to reduce acute ethanol intoxication. However, whereas glycine(B) site blockade potentiated ethanol intoxication, exogenous glycine(B) site activation failed to produce the hypothesized reduction in ethanol intoxication, perhaps because of saturating endogenous glycine levels (Debrouse et al., 2013). Other avenues to pursue could be the inhibition of the Akt/GSK3β signaling. Indeed inhibition of the Akt/GSK3β signaling by serotonin deficiency causes a reduced sensitivity to the intoxicating effect of ethanol (Sachs et al., 2014).
