The effects of hypoxia-ischemia on expression of c-Fos, c-Jun and Hsp70 in the young rat hippocampus

Krista L. Gilby, John N. Armstrong, R. William Currie, Harold A. Robertson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


The expression of c-Fos, c-Jun and Hsp70 was examined in the hippocampus at 6, 12, 24, 48, 72 h, 4, 7 and 42 days following a combination of unilateral common carotid artery ligation and 60 min of systemic hypoxia (8% oxygen, 92% nitrogen) in 25-day-old male rats. While pyknotic cells were not visible in the hippocampus of control animals, pyknosis was evident in the ipsilateral, but not the contralateral hippocampus, of hypoxic-ischemic animals beginning at 24 h post-hypoxia. Immunohistochemical analysis revealed no c-Fos-, c-Jun- or Hsp70-immunoreactivity (IR) in any control animals. However, at 6 h post-hypoxia, Fos- and Jun-IR was evident throughout the injured ipsilateral hippocampus and later appeared throughout the contralateral hippocampus, which never showed signs of pyknosis. In contrast, Hsp70-IR was first observed at 24 h post-hypoxia and was restricted to the injured ipsilateral hippocampus. Hsp70-IR was not, however, limited to dying neurons. H-I/seizure animals did not express these proteins at any time point. These results suggest that, even in irreversibly injured neurons, Fos, Jun and Hsp70 appear to be involved in the aftermath of ischemia but probably do not play a pivotal role in the outcome of H-I compromised cells. Furthermore, compounded injury (H-I/seizure) appears to block the synthesis these proteins.

Original languageEnglish (US)
Pages (from-to)87-96
Number of pages10
JournalMolecular Brain Research
Issue number1
StatePublished - Aug 1997
Externally publishedYes


  • Brain injury
  • Heat-shock protein
  • Hippocampus
  • Hypoxia-ischemia
  • Immediate-early gene
  • Stress

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


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