Growth retardation is the single most common deficit observed in infants exposed to ethanol in utero, and the molecular mechanisms responsible for this growth inhibition are a focus of ongoing research. Several lines of research have suggested that ethanol-induced changes in the adenylate cyclase-protein kinase cascade may be involved in this process. Using an embryonic chick model, it was demonstrated that ethanol exposure during early development caused increases in cellular prostaglandin E2 and cyclic AMP levels that were inversely correlated with brain weight. Paradoxically, basal adenylate cyclase and protein kinase catalytic activities, assayed in vitro, were not altered by ethanol dosing. Ethanol exposure did suppress the responsiveness of brain adenylate cyclase to exogenous PGE2. Furthermore, ethanol treatment significantly lowered the brain cytoplasmic levels of cyclic AMP binding protein.