Effect of Hypoxia-ischemia on c-fos Expression in the Neonatal Rat Brain

Lee, Wang Bock; Kwon, Sun Hak; Kim, Heng Mi

Abstract

PURPOSE: Brain damage resulting from a combination of hypoxia and ischemia in the newborn infant remains a major cause of perinatal death, cerebral palsy, mental retardation and epilepsy. Metabolic stress, including ischemia, hypoxia and seizures, induces the expression of a variety of stress proteins including nuclear proto-oncogene c-fos. The induction of c-fos can be considered a biomarker of events resulting from ischemia-hypoxia. However, it has been suggested that the mechanism for c-fos activation in the fetal brain is not mature prior to postnatal day 13-21. This study was undertaken to determine the induction of c-fos in neonatal rat brain by hypoxia-ischemia and the regions of brain most vulnerable to hypoxia-ischemia. MEHTODS: Ten-day-old postnatal rat pups, subjected to unilateral carotid artery dissection combined with 2-hour hypoxia, were killed at 2 hours and 6 hours after hypoxia-ischemia, and their brains were examined by immunohistochemistry.
RESULTS
Hypoxia-ischemia induced prominent expression of c-fos in the cingulate cortex and hippocampus in the postnatal rats 2 hours after the insult.
CONCLUSION
Hypoxia-ischemia results in increased c-fos expression in 10-day-old rat pups. The results of this experiment also demonstrate that the neonatal rat hippocampus and cortex are the most sensitive brain regions to the induction of c-fos following hypoxia-ischemia.