Persistent c-fos induction by nicotine in developing rat brain regions: interaction with hypoxia.

Published

Journal Article

Prenatal nicotine exposure evokes postnatal CNS cell loss. We administered nicotine to pregnant rats throughout gestation and neonatal brains were examined for expression of c-fos, a nuclear transcription factor involved in differentiation and cell death. The nicotine group showed persistent c-fos overexpression in the forebrain long after termination of exposure; in the brainstem, overexpression was apparent both after birth and at the end of the second postnatal week. In contrast to these effects, postnatal administration on d 1-4 caused persistent c-fos only at systemically toxic doses and treatment at subsequent ages did not cause induction at all. We also determined whether prenatal nicotine exposure would sensitize the brain to a subsequent postnatal episode of hypoxia comparable to that experienced during parturition. Hypoxia evoked acute stimulation of c-fos with a regional selectivity and ontogenetic profile differing from those of prenatal nicotine and this acute response was reduced by prenatal nicotine treatment. Persistent c-fos elevation is a harbinger of cell death, a relationship that provides an underlying mechanism for eventual cell deficits that appear after fetal nicotine exposure. Nicotine's interference with the acute c-fos stimulation caused by a subsequent episode of hypoxia may indicate a further compromise of cellular repair mechanisms.

Full Text

Duke Authors

Cited Authors

  • Trauth, JA; Seidler, FJ; McCook, EC; Slotkin, TA

Published Date

  • January 1999

Published In

Volume / Issue

  • 45 / 1

Start / End Page

  • 38 - 45

PubMed ID

  • 9890606

Pubmed Central ID

  • 9890606

International Standard Serial Number (ISSN)

  • 0031-3998

Digital Object Identifier (DOI)

  • 10.1203/00006450-199901000-00007

Language

  • eng

Conference Location

  • United States