Acute systemic ethanol administration directly alters PKC activity and expression in the brain (Kumar et al. 2006). However, ethanol administration to rats (2 g/kg) differentially alters PKCβ, γ, and ε expression and translocation to the P2 fraction of rat cerebral cortex (Kumar et al. 2006). PKCβ and PKCε expression in subcellular fractions exhibited responses to ethanol that likely represent increased synthesis and translocation, since increased levels of these kinases in the P2 fraction would require translocation of the enzyme. On the other hand, PKCγ expression and translocation to the P2 fraction of cortex are reduced by ethanol. These effects were associated with alterations in phosphorylation of both GABAA and NMDA receptors and/or associated proteins. Hence, ethanol differentially alters PKC expression in an isoform-specific manner and these effects are likely to contribute to GABAergic (and glutamatergic) actions of ethanol.
