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

Journal Article (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

International Standard Serial Number (ISSN)

  • 0031-3998

Digital Object Identifier (DOI)

  • 10.1203/00006450-199901000-00007


  • eng

Conference Location

  • United States