Abstract

Maternal tobacco smoking is the principal risk factor associated with sudden infant death syndrome (SIDS), a leading cause of death of infants under 1 year of age. Victims of SIDS show a higher incidence of respiratory control abnormalities, including central apnoeas, delayed arousal responses and diminished ventilatory chemoreflexes. Nicotine is likely the link between maternal tobacco smoking and SIDS. Prenatal nicotine exposure can alter the breathing pattern and can reduce hypoxia- and hypercarbia-induced ventilatory chemoreflexes. In vitro approaches have revealed that prenatal nicotine exposure impairs central chemosensitivity, switching the cholinergic contribution from a muscarinic to a nicotinic receptor-based drive. In addition, serotonergic, noradrenergic, GABAergic, glycinergic and glutamatergic, among others, are affected by prenatal nicotine. Here we propose that prenatal nicotine affects the respiratory network through two main processes: (i) reorganization of neurotransmitter systems; and (ii) remodelling of neural circuits. These changes make breathing more vulnerable to fail in early postnatal life, which could be related to the pathogenesis of SIDS. © 2009 Blackwell Publishing Asia Pty Ltd.