The reduction of the ethanol-induced suppression of γ oscillations by the PKA inhibitor H89 indicates the involvement of the PKA pathway in the ethanol effect at intoxicating concentrations, which is consistent with the report of acute ethanol induction of PKA activation (Naseer et al., 2010). The sensitivity of the ethanol effect to a DR1 antagonist suggest that the cAMP that drives PKA is in part due to the activation of DR1 (Rex et al., 2008), which are in area CA3 only expressed on interneurons (Gangarossa et al., 2012). Since ethanol causes an increase in dopamine release in the brain, this effect could even be stronger in vivo (Deng et al., 2009; Morikawa and Morrisett, 2010; Jerlhag et al., 2011; Theile et al., 2011).
