Effect of Hypoxia-ischemia on c-fos Expression in the Neonatal Rat Brain.
- Author:
Wang Bock LEE
1
;
Sun Hak KWON
;
Heng Mi KIM
Author Information
1. Department of Pediatrics, College of Medicine Kyungpook National University, Taegu, Korea.
- Publication Type:Original Article
- Keywords:
Hypoxia;
Ischemia;
Newborn rat;
c-fos
- MeSH:
Animals;
Anoxia;
Brain*;
Carotid Arteries;
Cerebral Palsy;
Epilepsy;
Gyrus Cinguli;
Heat-Shock Proteins;
Hippocampus;
Humans;
Immunohistochemistry;
Infant, Newborn;
Intellectual Disability;
Ischemia;
Proto-Oncogenes;
Rats*;
Seizures;
Stress, Physiological
- From:Journal of the Korean Pediatric Society
2000;43(3):386-394
- CountryRepublic of Korea
- Language:Korean
-
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.
