DEGRADATION OF FODRIN AND MAP-2 AFTER NEONATAL 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 m in) and allowed to recover for 3 h, 24 h, 2 days or 14 days. Consecuti ve tissue sections were stained with antibodies against alpha-fodrin, the 150 kDa breakdown product of alpha-fodrin (FBDP, marker of calpain proteolysis) or microtubule associated protein 2 (MAP 2, marker of de ndrosomatic neuronal injury). Cortical tissue pieces were subjected to Western blotting using the antibody against the FBDP. Areas with brai n injury displayed a distinct loss of MAP 2 which clearly delineated t he infarct. FBDP accumulated in injured and borderline regions ipsilat erally and a less conspicuous, transient increase in FBDP also occurre d in the contralateral hemisphere, especially in the white matter. A r eciprocal staining pattern could be seen in the cerebral cortex, i.e. loss of MAP 2 and accumulation of FBDP, most pronounced 14 days after the insult. Fodrin and MAP 2 are known calpain substrates, and degrada tion of these proteins preceded neuronal degeneration, indicating that these proteases may be involved in the early events triggering the ca scades leading to neuronal death.