ABSTRACT
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 epidemio-
logical findings show that exposure to tobacco smoke is now the number one risk
factor for the sudden infant death syndrome (SIDS), accounting for approxi-
mately one-third of all SIDS deaths (14,15). The major hypothesis addressed in
this chapter is that prenatal nicotine exposure enhances inhibitory neuro-
transmission, 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.
