Prenatal nicotine affects catecholamine gene expression in newborn rat carotid body and petrosal ganglion

Nicotine exposure modifies the expression of catecholamine and opioid neuro transmitter systems involved in attenuation of hypoxic chemosensitivity. We used in situ hybridization histochemistry to determine the effect of prena tal and early postnatal nicotine exposure on tyrosine hydroxylase (TH), dop amine beta -hydroxylase (D betaH), preproenkephalin (PPE), and D-2-dopamine receptor mRNA levels in the rat carotid body and petrosal ganglion during postnatal development. In the carotid body, nicotine increased TH mRNA expr ession in animals at 0 and 3 postnatal days (both, P < 0.05 vs. control) wi thout affecting TH mRNA levels at 6 and 15 days. At 15 postnatal days, D<be ta>H mRNA levels were increased in the carotid body of nicotine-exposed ani mals. Dopamine D-2-receptor mRNA levels in the carotid body increased with postnatal age but were unaffected by nicotine exposure. PPE was not express ed in the carotid body at any of the ages studied in control or treated ani mals. In the petrosal ganglion, nicotine increased the number of ganglion c ells expressing TH mRNA in animals at 3 days (P < 0.01 vs. control). D<beta >H mRNA expression was not induced nor was PPE mRNA expression increased in the petrosal ganglion in treated animals. Prenatal nicotine exposure upreg ulates mRNAs involved in the synthesis of two inhibitory neuromodulators, d opamine and norepinephrine, in peripheral arterial chemoreceptors, which ma y contribute to abnormalities in cardiorespiratory control observed in nico tine exposed animals.