Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats

T. A. Slotkin, Kent E Pinkerton, M. C. Garofolo, J. T. Auman, E. C. McCook, F. J. Seidler

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains and hearts were examined for alterations in adenylyl cyclase (AC) activity and for changes in β-adrenergic and m2-muscarinic cholinergic receptors and their linkage to AC. ETS exposure elicited induction of total AC activity as monitored with the direct enzymatic stimulant, forskolin. In the brain, the specific coupling of β-adrenergic receptors to AC was inhibited in the ETS groups, despite a normal complement of β-receptor binding sites. In the heart, ETS evoked a decrease in m2-receptor expression. In both tissues, the effects of postnatal ETS, mimicking passive smoking, were equivalent to (AC) or greater than (m2-receptors) those seen with prenatal ETS mimicking active smoking; the effects of combined prenatal and postnatal exposure were equivalent to those seen with postnatal exposure alone. These data indicate that ETS exposure evokes changes in cell signaling that recapitulate those caused by developmental nicotine treatment. Since alterations in AC signaling are known to affect cardiorespiratory function, the present results provide a mechanistic link reinforcing the participation of ETS exposure, including postnatal ETS, in disturbances culminating in events like Sudden Infant Death Syndrome.

Original languageEnglish (US)
Pages (from-to)73-81
Number of pages9
JournalBrain Research
Volume898
Issue number1
DOIs
StatePublished - Apr 13 2001

Fingerprint

Environmental Exposure
Adenylyl Cyclases
Smoke
Tobacco
Brain
Complement Receptors
Tobacco Smoke Pollution
Sudden Infant Death
Cholinergic Receptors
Muscarinic Receptors
Colforsin
Nicotine
Adrenergic Agents
Adrenergic Receptors
Smoking
Binding Sites
Pregnancy

Keywords

  • β-Adrenergic receptor
  • Adenylyl cyclase
  • Brain
  • Cholinergic receptor
  • Environmental tobacco smoke (ETS)
  • Heart
  • Nicotine
  • Sudden Infant Death Syndrome (SIDS)
  • Tobacco

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats. / Slotkin, T. A.; Pinkerton, Kent E; Garofolo, M. C.; Auman, J. T.; McCook, E. C.; Seidler, F. J.

In: Brain Research, Vol. 898, No. 1, 13.04.2001, p. 73-81.

Research output: Contribution to journalArticle

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abstract = "Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains and hearts were examined for alterations in adenylyl cyclase (AC) activity and for changes in β-adrenergic and m2-muscarinic cholinergic receptors and their linkage to AC. ETS exposure elicited induction of total AC activity as monitored with the direct enzymatic stimulant, forskolin. In the brain, the specific coupling of β-adrenergic receptors to AC was inhibited in the ETS groups, despite a normal complement of β-receptor binding sites. In the heart, ETS evoked a decrease in m2-receptor expression. In both tissues, the effects of postnatal ETS, mimicking passive smoking, were equivalent to (AC) or greater than (m2-receptors) those seen with prenatal ETS mimicking active smoking; the effects of combined prenatal and postnatal exposure were equivalent to those seen with postnatal exposure alone. These data indicate that ETS exposure evokes changes in cell signaling that recapitulate those caused by developmental nicotine treatment. Since alterations in AC signaling are known to affect cardiorespiratory function, the present results provide a mechanistic link reinforcing the participation of ETS exposure, including postnatal ETS, in disturbances culminating in events like Sudden Infant Death Syndrome.",
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