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

被引:39
作者
Frank, MG
Srere, H
Ledezma, C
O'Hara, B
Heller, HC
机构
[1] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA
[2] Stanford Univ, Dept Biol Sci, Stanford, CA 94305 USA
关键词
smoking; sleep; sudden infant death syndrome; cholinergic receptors;
D O I
10.1152/ajpregu.2001.280.4.R1134
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
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.
引用
收藏
页码:R1134 / R1140
页数:7
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