Effects of fetal nicotine exposure on development of adrenergic receptor binding in rat brain regions: Selective changes in α1 -receptors
Development of noradrenergic receptor binding capabilities was examined in brain regions of rats exposed to nicotine by continuous maternal infusion of 6 mg/kg/day from gestational day 4-20; this regimen produces regionally-selective alterations in presynaptic noradrenergic activity after birth. Nicotine exposure caused statistically significant increases in binding for the α1-receptor but not for the α2- or β-subtypes. The effect in the early neonatal period was not secondary to changes in presynaptic neural input, as the increase was apparent both in a region showing increased noradrenergic activity (midbrain + brainstem) and in one showing reduced activity (cerebral cortex). However, elevations in α1-receptor binding reappeared in young adulthood, a period in which nerve activity is subnormal in both regions in the nicotine group. These results suggest that prenatal exposure to nicotine causes a selective change in development of the α1-receptor that has both direct and nerve activity-related components.
