Perinatal exposure to nicotine causes deficits associated with a loss of nicotinic receptor function.

ABSTRACT: We investigated the role played by beta2-containing neuronal nicotinic receptors [nicotinic acetylcholine receptors (nAChRs)] in mediating nicotine's side effects in the fetus and newborn. Pregnant WT and mutant mice lacking the beta2 nAChR subunit were implanted with osmotic minipumps that delivered either water or a controlled dose of nicotine. Subsequently, we compared the development of the sympathoadrenal system and breathing and arousal reflexes of offspring shortly after birth, a period of increased vulnerability to nicotine exposure. Newborn WT pups exposed to nicotine exhibited all of the deficits associated with maternal tobacco and nicotine use, and linked to poor neonatal outcome: growth restriction, unstable breathing, and impaired arousal and catecholamine biosynthesis. Remar

SUBMITTER: Cohen G 

PROVIDER: S-EPMC552781 | biostudies-literature | 2005 Mar

REPOSITORIES: biostudies-literature