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Department of Pediatrics, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-3200
Nicotine exposure modifies
the expression of catecholamine and opioid neurotransmitter systems
involved in attenuation of hypoxic chemosensitivity. We used in
situ hybridization histochemistry to determine the effect of prenatal
and early postnatal nicotine exposure on tyrosine hydroxylase (TH),
dopamine
-hydroxylase (D
H), preproenkephalin (PPE), and
D2-dopamine receptor mRNA levels in the rat carotid body
and petrosal ganglion during postnatal development. In the carotid
body, nicotine increased TH mRNA expression in animals at 0 and 3 postnatal days (both, P < 0.05 vs. control) without
affecting TH mRNA levels at 6 and 15 days. At 15 postnatal days, D
H
mRNA levels were increased in the carotid body of nicotine-exposed animals. Dopamine D2-receptor mRNA levels in the carotid
body increased with postnatal age but were unaffected by nicotine
exposure. PPE was not expressed in the carotid body at any of the ages
studied in control or treated animals. In the petrosal ganglion,
nicotine increased the number of ganglion cells expressing TH mRNA in
animals at 3 days (P < 0.01 vs. control). D
H mRNA
expression was not induced nor was PPE mRNA expression increased in the
petrosal ganglion in treated animals. Prenatal nicotine exposure
upregulates mRNAs involved in the synthesis of two inhibitory
neuromodulators, dopamine and norepinephrine, in peripheral arterial
chemoreceptors, which may contribute to abnormalities in
cardiorespiratory control observed in nicotine exposed animals.
peripheral arterial chemoreceptors; tyrosine hydroxylase; dopamine
-hydroxylase; preproenkephalin; control of breathing; sudden infant
death syndrome
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