This chapter considers the influence of prenatal nicotine exposure on the development of neurotransmission in central respiratory neurons. Neonatal mammals that are nicotine exposed in utero show abnormalities in central ventilatory control, such as reduced ventilatory output (1,2), altered breathing pattern (2-4), increased apnea frequency (2,4) and duration (5), delayed arousal in response to hypoxia (6,7), decreased sensitivity to hypoxia (1,4,5,8-11), and diminished capacity for autoresuscitation following severe hypoxic exposure (12,13). Although these findings provide substantial evidence that development of central ventilatory control is altered by prenatal nicotine exposure, the mechanism of nicotine’s action on respiratory-related neurons has not been identified. Identifying these mechanisms is important clinically, as epidemiological findings show that exposure to tobacco smoke is now the number one risk factor for the sudden infant death syndrome (SIDS), accounting for approximately one-third of all SIDS deaths (14,15). The major hypothesis addressed in this chapter is that prenatal nicotine exposure enhances inhibitory neurotransmission, and may also depress excitatory neurotransmission. It is envisaged that these alterations make the neonate more vulnerable to exogenous stressors, such as hypoxia, hypercapnia, asphyxia, and laryngeal irritation. The increased vulnerability is likely manifest as a diminution of protective reflex responses to these stressors, leading to life-threatening events.
|Original language||English (US)|
|Title of host publication||Sleep and Breathing in Children|
|Subtitle of host publication||Developmental Changes in Breathing During Sleep, Second Edition|
|Number of pages||139|
|State||Published - Jan 1 2008|
ASJC Scopus subject areas