Exposure to tobacco smoke during pregnancy is associated with a range of adverse outcomes in offspring, including cognitive deficits and increased incidence of attention deficit-hyperactivity disorder, but there is a considerable controversy with regard to the causal role of tobacco smoke in these outcomes. To determine whether developmental exposure to the primary psychoactive ingredient in tobacco smoke, nicotine, may cause long-lasting behavioral alterations analogous to those in attention deficit-hyperactivity disorder, male Sprague-Dawley rats underwent a chronic neonatal nicotine administration regimen, which models third-trimester human exposure. Male rat pups were administered nicotine (6 mg/kg/day) by oral gastric intubation on postnatal days 1-7. In adulthood, rats were tested in two decision-making tasks (risky decision-making and delay discounting) as well as in free-operant responding for food reward and the elevated plus maze. Chronic neonatal nicotine attenuated weight gain during nicotine exposure, but there were no effects on performance in the decision-making task, and only a modest decrease in arm entries in the elevated plus maze in one subgroup of rats. These data are consistent with previous findings that developmental nicotine exposure has no effect on delay discounting, and they extend these findings to risky decision-making as well. They further suggest that at least some neurocognitive alterations associated with prenatal tobacco smoke exposure in humans may be due to genetic or other environmental factors, including non-nicotine components of tobacco smoke.