This study determined the effects of prenatal nicotine exposure (2 mg/kg/day) in Sprague-Dawley CD rats via subcutaneously implanted osmotic minipumps, during gestational days 7-21, on postnatal levels of neuronal nicotinic receptor α4, α7 and β2 subunit messenger RNAs. Northern analysis of postnatal day 1, 7, 14 and 28 hippocampal/septal and cortical total RNA using α-[32P]dCTP-labeled α4, α7 and β2 complementary DNA probes identified a single (5.7-kb) α7 messenger RNA, three (2.4-, 3.8- and 8.0- kb) α4 messenger RNAs and four (3.7-, 5.0-, 7.5- and 10.0-kb) β2 messenger RNAs. In comparison to prenatal saline, prenatal nicotine produced several significantly higher messenger RNA levels (cortical: 5.7-kb α7, 2.4-, 3.8- and 8.0-kb α4, 10.0-kb β2; hippocampal/septal: 2.4- and 8.0-kb α4); these increases occurred predominantly on, but were not restricted to, postnatal day 14. Effects of nicotine were generally resolved by postnatal day 28. Collapsing the data across sex and age, a significant treatment effect indicated that hippocampal/septal and cortical 8.0-kb α4 messenger RNA levels and 10.0-kb β2 messenger RNA levels were significantly higher following prenatal nicotine exposure. This is the first study indicating that prenatal nicotine produces alterations in developing postnatal rat neuronal nicotinic receptor messenger RNA levels, possibly by premature stimulation of neuronal nicotinic receptors. These results further implicate the teratogenic potential of nicotine in postnatal neuronal development.