Long-Evans lactating rats were fed 27% calories as ethanol in a liquid diet to determine whether alcohol received through the milk would alter normal brain development in the offspring. On days 16, 21 and 30, brains of the female offspring were removed, corpus striatum dissected and assayed for choline acetyltransferase activity, glutamic acid decarboxylase activity and [3H]spiroperidol binding activity. At day 16, there were no differences among the three treatment groups for the enzyme activities assayed. At day 21, glutamic acid decarboxylase activity in the pairfed group was higher than in ET and CT groups. Choline acetyltransferase activity in PF group was higher when compared to ad libitum controls and [3H]spiroperidol binding was not affected. At 30 days of age, animals exposed to ethanol had higher choline acetyltransferase activity and [3H]spiroperidol binding activity when compared to pairfed and ad libitum controls; and higher glutamic acid decarboxylase activity when compared to ad libitum controls. Data from the present study suggest that ethanol exposure during the brain growth spurt has a toxic effect on the late development of dopaminergic, cholinergic and GABAergic systems in the corpus striatum. These results may be related to the clinical symptoms of hyperactivity and problems with motor control in children exposed to alcohol during the third trimester and during lactation.