Effect of prenatal and postnatal ethanol exposure on Ca2+ /calmodulin-dependent protein kinase II in rat cerebral cortex.

The ability of ethanol to influence Ca2+ /calmodulin-dependent protein kinase II (CaM kinase II)-mediated phosphorylation in rat cerebral cortex during prenatal and postnatal ethanol treatment was examined. Ethanol treatment increased protein expression of CaM kinase II alpha-subunit in membrane and cytosolic fractions during development. When specific CaM kinase II stimulators (Ca2+ /calmodulin) and inhibitor (autocamtide-2-related inhibitory peptide) were included during in vitro phosphorylation assays, three putative proteins (65, 50, and 40 kDa) were specifically phosphorylated by CaM kinase II, which might be involved in neurosignaling events associated with chronic ethanol treatment. Given that activation of CaM kinase II is a prerequisite for long-term potentiation induction through N-methyl-D-aspartate receptors, ethanol-induced increase in the levels of CaM kinase II alpha-subunit and selective phosphorylation of specific substrate proteins in cerebral cortex suggest a relation between calcium influx and increased CaM kinase II levels that might be relevant in ethanol-induced central nervous system dysfunction.