Abstract
Human and animal studies have conclusively shown that prenatal nicotine exposure alters fetal brain development and causes persistent impairment in the cognitive function of offspring. However, the mechanisms underlying the effect of prenatal nicotine exposure on cognitive function in offspring are still unclear. The objective of this review is to discuss the published studies on the mechanisms underlying the effects of prenatal nicotine exposure on cognitive impairment and discuss the potential mechanisms of action. The findings of the reviewed studies show that the main mechanisms involved are alteration in the composition of nicotinic acetylcholine receptor subunits, increase in surface expression of the glutamate receptor subunit GluR2, a reduction in neurogenesis, alteration of Akt and ERK1/2 activity, and mitochondrial dysfunction in the hippocampus and cortex. These pathways could shed light on future molecular markers and therapeutic targets for the prevention and treatment of cognitive dysfunction induced by prenatal nicotine exposure.