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Am J Physiol Regul Integr Comp Physiol 280: R1134-R1140, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 4, R1134-R1140, April 2001

Prenatal nicotine alters vigilance states and AchR gene expression in the neonatal rat: implications for SIDS

Marcos G. Frank2, Hilary Srere1, Carlos Ledezma1, Bruce O'Hara1, and H. Craig Heller1

1 Department of Biological Sciences, Stanford University, Stanford 94305; and 2 Department of Physiology, University of California at San Francisco, San Francisco, California 94143

Maternal smoking is a major risk factor for sudden infant death syndrome (SIDS). The mechanisms by which cigarette smoke predisposes infants to SIDS are not known. We examined the effects of prenatal nicotine exposure on sleep/wake ontogenesis and central cholinergic receptor gene expression in the neonatal rat. Prenatal nicotine exposure transiently increased sleep continuity and accelerated sleep/wake ontogeny in the neonatal rat. Prenatal nicotine also upregulated nicotinic and muscarinic cholinergic receptor mRNAs in brain regions involved in regulating vigilance states. These findings suggest that the nicotine contained in cigarette smoke may predispose human infants to SIDS by interfering with the normal maturation of sleep and wake.

smoking; sleep; sudden infant death syndrome; cholinergic receptors


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