Previously we observed that chronic nicotine-treated adult rats developed locomotor hyperactivity which was mediated by changes in nicotinic and dopaminergic receptors in the striatum. In this study, we further examined if such changes would also occur in pups that were prenatally exposed to nicotine. Fourteen-day-old offspring from dams which were implanted with osmotic minipumps containing nicotine (1.5 mg/kg/day) throughout the entire gestational period were employed in this investigation. Prenatal nicotine treatment lowered the number of male pups born and reduced the postnatal gain in body weight and length of both male and female offspring. Prenatal exposure to nicotine did not alter the motor coordination of the pups. A decrease in the number of striatal dopaminergic receptor binding sites (Bmax) was detected in the male pups, however an increase in the ligand affinity to the receptors (1/KD) had been simultaneously detected. No change in the characteristics of nicotinic receptor binding sites and the levels of dopamine and its metabolite, 3,4-dihydroxyphenylacetic acid was found in the striatal region. The present study indicates that prenatal exposure to nicotine may cause changes in growth and development of the animals. However, in comparison to chronic nicotine-treated adult rats, prenatal exposure to nicotine had only modified the dopaminergic receptor system in the striatal region of male offspring.