This review examines the evidence that glucocorticoids are involved, during both adolescence and adulthood, in the cognitive deficits caused by long-term alcohol consumption and in the mechanism(s) of alcohol dependence. During adolescence, the hypothalamopituitary-adrenal (HPA) axis undergoes well-characterized changes in basal activity and many of these are influenced by alcohol consumption. While the former have been fairly well studied, there is little information about whether alcohol effects on the HPA in adolescents differ from those in adults. The means by which glucocorticoids may influence alcohol-related neurotoxicity are presented, and potential differences between adolescence and adults in this regard noted. The substantial evidence for involvement of glucocorticoids in alcohol-induced cognitive deficits is described, with particular reference to the consequences of alcohol withdrawal. The use of immature organotypic cultures of rodent brain in the study of alcohol neurotoxicity is considered in detail, and the information obtained from this methodology concerning the role of glucocorticoid receptors and excitable membrane proteins in this neurotoxicity. The influence of glucocorticoids on alcohol consumption and possible contributions to alcohol dependence are then considered. In conclusion, more information concerning the effects of glucocorticoids on plasticity and alcohol neurotoxicity during the adolescent period is needed.