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

Abstract

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.

Prenatal to Early Postnatal Nicotine Exposure Impairs Central Chemoreception and Modifies Breathing Pattern in Mouse Neonates: A Probable Link to Sudden Infant Death Syndrome

“…To identify the particular subtypes of muscarinic and of nicotinic receptors that were altered by prenatal nicotine exposure would require pharmacological tools in addition to atropine and hexamethonium, used in this study. Prenatal nicotine exposure can reduce muscarinic receptor actions through uncoupling of G-protein dependent mechanisms, as described in rat striatum and hippocampus (Zahalka et al, 1993), or by reducing the binding of M2 muscarinic receptors in the rat brainstem at an early postnatal period (Slotkin et al, 1999), or by reducing mRNA of the muscarinic receptor in basal ganglia (Frank et al, 2001). However, it can increase nicotinic actions by receptor upregulation as described in the brainstem and cerebellum of rats .…”

Alterations in cholinergic sensitivity of respiratory neurons induced by pre-natal nicotine: a mechanism for respiratory dysfunction in neonatal mice

“…Pre-natal nicotine reduces the binding of M2 muscarinic receptors in the rat brainstem at early post-natal periods (Slotkin et al 1999). In other systems, pre-natal nicotine can alter muscarinic receptor actions, either by uncoupling G-protein-dependent mechanisms in rat striatum and hippocampus (Zahalka et al 1993) or by reducing mRNA of the muscarinic receptor in basal ganglia (Frank et al 2001). Chronic nicotine exposure may lead to desensitization of nAChRs (Wang & Sun 2005) or their upregulation (Gaimarri et al 2007).…”

Central cholinergic regulation of respiration: nicotinic receptors

“…In animal studies, prenatal exposure to nicotine affects neuronal development and upregulates nAChRs in the brain [102][103][104][105] . Prenatal exposure to nicotine impairs protective responses to hypoxia in an age-dependent manner in rat pups [106] .…”