Biochemical studies have confirmed that nicotinic acetylcholine receptor mRNA and protein are expressed early in the development of the fetal central nervous system. Perinatal administration of nicotine produces a broad spectrum of effects on brain development, including inhibition of DNA synthesis, altered ornithine decarboxylase activity, altered neurotransmitter function, and significant alterations in cortical morphogenesis. Catecholamine systems, both in the brain and in the periphery, are particularly sensitive to prenatal nicotine exposure. Acute and chronic nicotine administered to pregnant dams causes alterations in dopamine and its metabolites in male and female rat fetuses. These changes can persist into adulthood. Prenatal nicotine exposure also causes locomotor disturbances in pups, which can have long-lasting effects. The effect of nicotine on developing noradrenergic neurons is less clear. Some effects may include increases in noradrenergic neuronal activity in the pup and aberrant central release of norepinephrine in response to neonatal hypoxia after nicotine exposure in utero. Catecholamine neurons develop early in ontogeny, so nicotine induced alterations have the potential to induce permanent changes. Hence, more research is needed to get a clearer picture of the effect of nicotine on developing catecholamine systems. The affects of nicotine on catecholamine systems in the adult are discussed for comparison.