In animal models, exposure to cigarette smoke or nicotine during fetal development
alters the expression of the nicotinic acetylcholine receptor in areas of the brainstem important for autonomic function, 28
alters the neuronal excitability of neurons in the nucleus tractus solitarius (a brainstem region important for sensory integration), 29 and
alters fetal autonomic activity and medullary neurotransmitter receptors.30 In human infants, there are strong associations between nicotinic acetylcholine receptor and serotonin receptors in the brainstem during development.31 Prenatal exposure to tobacco smoke attenuates recovery from hypoxia in preterm infants, 32 decreases heart rate variability in preterm33 and term34 infants, and abolishes the
normal relationship between heart rate and gestational
age at birth.33 Moreover, infants of smoking mothers exhibit impaired arousal patterns to trigeminal stimulation in proportion to urinary cotinine levels.35 It is important to note also that prenatal exposure to tobacco smoke
alters the
normal programming of cardiovascular reflexes such that there is a greater - than - expected increase in blood pressure and heart rate in response to breathing 4 % carbon dioxide or a 60 ° head - up tilt.36 These changes in autonomic function, arousal, and cardiovascular reflexes might all increase an infant's vulnerability to SIDS.
While
normal RNA regulation involves regulated and reversible assembly of RNA - protein particles, both increased cellular
age and mutation push the process towards hyperassembly, which leads to
altered pools of RNA or RNA regulatory proteins in neurons that contribute to their eventual death.