We studied the involvement of altered noradrenergic function in the behavioral consequences of fetal ethanol exposure. Pregnant rats were fed a liquid diet containing 35% Ethanol-Derived Calories (EDC), pair-fed a 0% EDC diet with sucrose substituted isocalorically for ethanol, or fed ad lib lab chow. In Experiment 1, offspring from these prenatal treatment groups were injected with the alpha-adrenergic agonist clonidine (0.5 or 2.0 mg/kg) at 10 or 42 days of age and showed age-characteristic, dose-dependent increases in locomotor activity, exploration, forelimb treading, and catalepsy. In Experiment 2, offspring were injected with clonidine (0.25 or 1.0 mg/kg) at 10, 14, or 18 days of age, and locomotor activity and wall-climbing were observed in a warm chamber (33 degrees C). Catalepsy and rectal temperature were also scored. There were no significant differential effects of clonidine on any prenatal treatment group at any age for any measure of activity or rectal temperature. The results do not support the hypothesis that fetal ethanol exposure alters noradrenergic systems in behaviorally significant ways.