THE EFFECTS OF HYPOXIA-ISCHEMIA ON EXPRESSION OF C-FOS, C-JUN AND HSP70 IN THE YOUNG-RAT HIPPOCAMPUS

The expression of c-Fos, c-Jun and Hsp70 was examined in the hippocamp us at 6, 12, 24, 48, 72 h, 4, 7 and 42 days following a combination of unilateral common carotid artery ligation and 60 clin of systemic hyp oxia (8% oxygen, 92% nitrogen) in 25-day-old male rats. While pyknotic cells were not visible in the hippocampus of control animais, pyknosi s was evident in the ipsilateral, but not the contralateral hippocampu s, of hypoxic-ischemic animals beginning at 24 h post-hypoxia. Immunoh istochemical analysis revealed no c-Fos-, c-Jun- or Hsp70-immunoreacti vity (IR) in any control animals. However, at 6 h post-hypoxia, Fos- a nd Jun-IR was evident throughout the injured ipsilateral hippocampus a nd later appeared throughout the contralateral hippocampus, which neve r showed signs of pyknosis. In contrast, Hsp70-IR was first observed a t 24 h post-hypoxia and nas restricted to the injured ipsilateral hipp ocampus. Hsp70-IR was not, however, limited to dying neurons. H-I/seiz ure animals did not express these proteins at any time point. These re sults 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. F urthermore, compounded injury (H-I/seizure) appears to block the synth esis these proteins.