Prenatal nicotine alters nicotinic receptor development in the mouse brain.

Maternal smoking during pregnancy may affect development of the child, but little is known about potential mechanisms of these effects. Since chronic nicotine treatment alters brain nicotinic receptors in adults and also evokes tolerance which is regulated by genetic factors, pregnant mice of two inbred strains underwent chronic nicotine infusion to determine whether the developmental pattern of mouse brain nicotinic receptors would be altered. C3H/2ibg and C57BL/6ibg mice were infused SC with saline or 2.0 mg/kg/h nicotine during the last half of pregnancy. The developmental profiles of [3H]nicotine and alpha-[125I]bungarotoxin binding in seven brain regions obtained from the offspring were measured. Prenatal nicotine treatment increased levels of [3H]nicotine binding at birth in the C3H hypothalamus, hippocampus, and possibly the cortex, and in the C57BL cortex. At later ages (20-30 days), [3H]nicotine binding was elevated in the C3H hindbrain, hippocampus, striatum, midbrain, and possibly the cortex. The C57BL hindbrain, hippocampus, midbrain, and cortex also showed increased binding at 20-30 days. Little, if any, effect of prenatal nicotine treatment was observed on the development of the alpha-[125I]bungarotoxin binding site. Since upregulated [3H]nicotine binding returns to control levels in adult animals within seven days following termination of chronic nicotine infusion, it is unlikely that simple upregulation is responsible for the changes observed in 20-30-day-old mouse brains.