NMDAR stimulation can activate Akt via PI3-kinase signaling (Perkinton et al., 2002; Crossthwaite et al., 2004). Interestingly, Akt can be also activated via dopamine receptor mediated cAMP-PKA signaling, a PI3-kinase independent mechanism (Filippa et al., 1999; Brami-Cherrier et al., 2002). Since blocking PI3-kinase had no effect on ethanol-induced suppression of γ oscillations, Akt activation is likely through DR-PKA signaling (Filippa et al., 1999; Brami-Cherrier et al., 2002). The initial increase in γ power and the complete occlusion of the ethanol-induced suppression of γ oscillations by an Akt inhibitor suggests that Akt activation, due to acute ethanol exposure (Neasta et al., 2011; Zeng et al., 2012) inhibits γ-generating network through yet unknown pathways (Figure 7).
