PRENATAL NICOTINE EXPOSURE AND COGNITIVE PERFORMANCE IN RATS

In humans and animal models there is evidence that prenatal nicotine e xposure causes lasting deficits in cognitive performance. The current study examined the cognitive effects of prenatal exposure of rats to 2 mg/kg/day of nicotine. This dose did not cause significant deficits i n maternal weight gain, offspring litter size, or pup weight. The cont rol offspring showed the normal ontogeny of spontaneous alternation fr om near chance (50%) performance to 80%-85% alternation. In contrast, the nicotine-exposed rats had the opposite progression with abnormally high alternation on days 22-30 and abnormally low alternation on days 35-52. Acquisition of choice accuracy performance on the radial-arm m aze (RAM) was not altered in a major way by nicotine exposure. Minor n icotine-induced changes in choice accuracy were seen during the initia l trials of acquisition. The nicotine ''posed female offspring had a s ignificantly longer response duration. Prenatal nicotine exposure did significantly alter the effects of subsequent drug challenges on choic e accuracy performance. The nicotine-exposed male offspring were signi ficantly more responsive to the amnestic effects of the nicotinic anta gonist mecamylamine. In a subsequent challenge, the effects of the bet a-adrenergic antagonist propranolol were examined. A significant dose- related impairment in choice accuracy was seen in the control rats. In contrast, the nicotine-exposed rats did not show any significant resp onse to propranolol. This decreased responsiveness to adrenergic chall enge parallels the reduction in adrenergic response to nicotine challe nge we previously found in littermates to the rats of the current stud y. Prenatal nicotine exposure causes subtle alterations in cognitive p erformance that can be magnified by challenges of nicotinic and adrene rgic systems.