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

Estelle B. Gauda, Reed Cooper, Patrice K. Akins, Guimei Wu

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


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 β-hydroxylase (DβH), 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, DβH 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). DβH 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.

Original languageEnglish (US)
Pages (from-to)2157-2165
Number of pages9
JournalJournal of applied physiology
Issue number5
StatePublished - 2001
Externally publishedYes


  • Control of breathing
  • Dopamine β-hydroxylase
  • Peripheral arterial chemoreceptors
  • Preproenkephalin
  • Sudden infant death syndrome
  • Tyrosine hydroxylase

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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