Accumulating evidence indicates that the cyclic adenosine monophosphate (cAMP)-dependent kinase PKA is involved in the neurobiological responses to ethanol. PKA is a tetramer composed of a regulatory homodimer and two catalytic subunits. PKA activation occurs when cAMP binds to the regulatory subunits of the PKA complex, liberating the catalytically active subunits, which diffuse throughout the cell and phosphorylate nearby proteins. Ethanol stimulates cAMP signaling through activation of adenosine A2a receptors. Since A2a receptors are coupled to stimulatory G proteins, this increases levels of intracellular cAMP followed by stimulation of PKA (see Diamond and Gordon 1994 for review). Recently, we have found that acute ethanol exposure increases the expression of PKA regulatory RIIα and RIIβ subunits in the membrane fraction of rat cerebral cortex and also alters GABAA receptor expression (Kumar et al. 2008). Therefore, it appears that ethanol alters PKA expression in a subunit specific manner and may affect GABAA receptor expression.
