Acute and chronic ethanol consumption effects on the immunolabeling of G(q/11 alpha) subunit protein and phospholipase C isozymes in the rat brain

The goal of this investigation was to examine whether postreceptor sites [G(q/11) protein and phospholipase C (PLC) isozymes] of the phosphoinositide signal transduction system are involved in neuroadaptational mechanisms in the brain during chronic ethanol consumption. It was observed that acute ethanol treatment has no effect on the immunolabeling of PLC-beta(1), -gamma(1), and -delta(1) and the a subunit of G(q/11) protein in the rat cortex as determined by western blotting using specific monoclonal antibodies. On the other hand, chronic ethanol consumption (15 days) resulted in a significant decrease in the immunolabeling of PLC-beta(1), whereas under identical conditions, the immunolabeling of PLC-gamma(1) and -delta(1) isozymes was not significantly altered. The decreased immunolabeling of PLC-beta(1) during chronic ethanol consumption was not altered by 24 h of withdrawal after 15 days of ethanol consumption. The immunolabeling of the a subunit of G(q/11) protein was significantly decreased after 15 days of ethanol consumption but had returned to normal levels after 24 h of ethanol withdrawal. Also, chronic ethanol treatment resulted in a significant decrease in phosphatidylinositol 4,5-bisphosphate-specific PLC activity, which remained the same after 24 h of ethanol withdrawal. These results suggest that decreased PLC activity during ethanol consumption and its withdrawal may be due to decreased protein levels of the G(q/11) protein-coupled PLC-beta(1) isozyme but not the PLC-gamma(1) or -delta(1) isozyme in the rat cortex. It is possible that changes in the protein levels of the G(q/11) protein-coupled PLC-beta(1) isozyme and in PLC activity in the brain may be involved in the cellular adaptation to chronic ethanol exposure.