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 sit es [G(q/11) protein and phospholipase C (PLC) isozymes] of the phospho inositide signal transduction system are involved in neuroadaptational mechanisms in the brain during chronic ethanol consumption. It was ob served that acute ethanol treatment has no effect on the immunolabelin g 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 sp ecific monoclonal antibodies. On the other hand, chronic ethanol consu mption (15 days) resulted in a significant decrease in the immunolabel ing of PLC-beta(1), whereas under identical conditions, the immunolabe ling of PLC-gamma(1) and -delta(1) isozymes was not significantly alte red. The decreased immunolabeling of PLC-beta(1) during chronic ethano l consumption was not altered by 24 h of withdrawal after 15 days of e thanol consumption. The immunolabeling of the a subunit of G(q/11) pro tein was significantly decreased after 15 days of ethanol consumption but had returned to normal levels after 24 h of ethanol withdrawal. Al so, chronic ethanol treatment resulted in a significant decrease in ph osphatidylinositol 4,5-bisphosphate-specific PLC activity, which remai ned the same after 24 h of ethanol withdrawal. These results suggest t hat decreased PLC activity during ethanol consumption and its withdraw al may be due to decreased protein levels of the G(q/11) protein-coupl ed PLC-beta(1) isozyme but not the PLC-gamma(1) or -delta(1) isozyme i n 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 i n the brain may be involved in the cellular adaptation to chronic etha nol exposure.