Eb. Gauda et al., Prenatal nicotine affects catecholamine gene expression in newborn rat carotid body and petrosal ganglion, J APP PHYSL, 91(5), 2001, pp. 2157-2165
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.