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

Citation
Ta. Trauth et al., Persistent c-fos induction by nicotine in developing rat brain regions: Interaction with hypoxia, PEDIAT RES, 45(1), 1999, pp. 38-45
Citations number
69
Categorie Soggetti
Pediatrics,"Medical Research General Topics
Journal title
PEDIATRIC RESEARCH
ISSN journal
00313998 → ACNP
Volume
45
Issue
1
Year of publication
1999
Pages
38 - 45
Database
ISI
SICI code
0031-3998(199901)45:1<38:PCIBNI>2.0.ZU;2-9
Abstract
Prenatal nicotine exposure evokes postnatal CNS cell loss. We administered nicotine to pregnant rats throughout gestation and neonatal brains were exa mined for expression of c-fos, a nuclear transcription factor involved in d ifferentiation and cell death. The nicotine group showed persistent c-fos o verexpression in the forebrain long after termination of exposure; in the b rainstem, overexpression was apparent both after birth and at the end of th e second postnatal week. In contrast to these effects, postnatal administra tion on d 1-4 caused persistent c-fos only at systemically toxic doses and treatment at subsequent ages did not cause induction at ail. We also determ ined whether prenatal nicotine exposure would sensitize the brain to a subs equent postnatal episode of hypoxia comparable to that experienced during p arturition. Hypoxia evoked acute stimulation of c-fos with a regional selec tivity and ontogenetic profile differing from those of prenatal nicotine an d this acute response was reduced by prenatal nicotine treatment. Persisten t c-fos elevation is a harbinger of cell death, a relationship that provide s an underlying mechanism for eventual cell deficits that appear after feta l nicotine exposure. Nicotine's interference with the acute c-fos stimulati on caused by a subsequent episode of hypoxia may indicate a further comprom ise of cellular repair mechanisms.