Cigarette smoke exposure effects on the brainstem expression of nicotinic acetylcholine receptors (nAChRs), and on cardiac, respiratory and sleep physiologies.

Cigarette smoking during pregnancy is the largest modifiable risk factor for adverse outcomes in the infant. Investigations have focused on the psychoactive component of cigarettes, nicotine. One proposed mechanism leading to adverse effects is the interaction between nicotine and its nicotinic acetylcholine receptors (nAChRs). Much data has been generated over the past three decades on the effects of cigarette smoke exposure (CSE) on the expression of the nAChRs in the brainstem and physiological parameters related to cardiac, respiration and sleep, in the offspring of smoking mothers and animal models of nicotine exposure. This review summarises this data and discusses the main findings, highlighting that findings in animal models closely correlate with those from human studies, and that the major brainstem sites where the expression level for the nAChRs are consistently affected include those that play vital roles in cardiorespiration (hypoglossal nucleus, dorsal motor nucleus of the vagus, nucleus of the solitary tract), chemosensation (nucleus of the solitary tract, arcuate nucleus) and arousal (rostral mesopontine sites such as the locus coeruleus and nucleus pontis oralis). These findings provide evidence for the adverse effects of CSE during and after pregnancy to the infant and the need to continue with the health campaign advising against CSE.