FODRIN DEGRADATION AND SUBCELLULAR-DISTRIBUTION OF CALPAINS AFTER NEONATAL RAT CEREBRAL HYPOXIC-ISCHEMIA

Neonatal rats were subjected to transient cerebral hypoxic-ischemia (u nilateral occlusion of the common carotid artery +7.70% O-2 for 100 mi n). Ipsi-and contralateral parietal cerebral cortex was assayed with W estern blotting for fodrin breakdown product (FBDP). Calpain immunorea ctivity was assayed in the cytosolic fraction (CF) and the membrane an d microsomal fraction (MMF). Calpain immunoreactivity decreased bilate rally in the CF during the insult (62-68% of controls) and remained si gnificantly lower during early recovery, whereas the MMF showed no sig nificant changes. This relative redistribution of calpains coincided w ith the appearance of FBDP in the left, ipsilateral hemisphere, displa ying a significantly higher level of FBDP from immediately after the i nsult until at least 1 day of recovery (204-292% of controls). No sign ificant changes in FBDP could be detected in the right, contralateral hemisphere, indicating that although redistribution of calpains occurr ed, hypoxia per se did not suffice to initiate fodrin degradation in t his model of neonatal hypoxic-ischemia.