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Vol. 285, Issue 3, 931-945, June 1998
Department of Pharmacology and Cancer Biology, Duke University
Medical Center, Durham, North Carolina
Despite extensive adverse publicity, tobacco use continues in
approximately 25% of all pregnancies in the United States,
overshadowing illicit drugs of abuse, including cocaine. The societal
cost of maternal smoking is seen most readily in underweight newborns, in high rates of perinatal morbidity, mortality and Sudden Infant Death
Syndrome and in persistent deficits in learning and behavior. We have
designed animal models of nicotine exposure to prove that nicotine
itself is a neuroteratogen, thus providing a causative link between
tobacco exposure and adverse perinatal outcomes. In particular,
nicotine infusion paradigms that, like the transdermal patch used in
man, produce drug exposure without the confounds of other components of
tobacco or of episodic hypoxic-ischemic insult, have enabled a
mechanistic dissection of the role played by nicotine in fetal brain
damage. Nicotine targets specific neurotransmitter receptors in the
fetal brain, eliciting abnormalities of cell proliferation and
differentiation, leading to shortfalls in the number of cells and
eventually to altered synaptic activity. Because of the close
regulatory association of cholinergic and catecholaminergic systems,
adverse effects of nicotine involve multiple transmitter pathways and
influence not only the immediate developmental events in fetal brain,
but also the eventual programming of synaptic competence. Accordingly,
defects may appear after a prolonged period of apparent normality,
leading to cognitive and learning defects that appear in childhood or
adolescence. Comparable alterations occur in peripheral autonomic
pathways, leading to increased susceptibility to hypoxia-induced brain
damage, perinatal mortality and Sudden Infant Death. Identifying the
receptor-driven mechanisms that underlie the neurobehavioral damage
caused by fetal nicotine exposure provides a rational basis for
decisions about nicotine substitution therapy for smoking cessation in
pregnancy. In contrast to the effects of nicotine, animal models of
crack cocaine use in pregnancy indicate a more restricted spectrum of
effects, a reflection of differences both in pharmacokinetics and
pharmacodynamics of the two drugs. Notably, although cocaine, like
nicotine, also targets cell replication, its effects are short-lived,
permitting recovery to occur in between doses, so that the eventual
consequences are much less severe. To some extent, the effects of
cocaine on brain development resemble those of nicotine because the two
share cardiovascular actions (vasoconstriction) that, under some
circumstances, elicit fetal hypoxia-ischemia. In light of the fact that
nearly all crack cocaine users smoke cigarettes, the identification of
specific developmental effects of cocaine may prove difficult to
detect. Although scientists and the public continue to pay far more
attention to fetal cocaine effects than to those of nicotine or tobacco use, a change of focus to concentrate on tobacco could have a disproportionately larger impact on human health.
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