Cytoskeletal proteins are important in maintaining neuronal structural integrity and in axonal transport. Changes in the amount of these proteins may be the first manifestation of neuronal injury. We examined the effect of cerebral hypoxia-ischemia (HI) on 3 cytoskeletal proteins, neurofilament (NF) 68 kD, NF 200 kD and class III β-tubulin (tub). Methods: Anesthetized immature rabbits were subjected to HI (n=9) by breathing 2.5% O2 for 8 min followed by 8 min of ischemia. Ischemia was produced by raising intracranial pressure equal to mean arterial pressure by infusing a mock CSF into the subarachnoid space. After 4 hr of reperfusion, the cytoskeletal proteins were measured in 5 brain regions using dot-immunoblotting. Sham-operated control rabbits (n=8) were evaluated for an equivalent time period. Statistical analysis used a repeated measures ANOVA.Results: At 4 hr, NF 68 kD was lower (p<0.05) in the HI group. However, NF 200 kD was significantly elevated (p<0.001). There was no(p>0.05) interaction between region and group for either NF protein. Tub was similar in the groups (p>0.05). Conclusion: Both NF 68 kD and NF 200 kD proteins are altered after HI. While NF 68 kD is reduced, NF 200 kD is unexpectedly elevated. Since the assay used to measure these proteins is not affected by the state of NF phosphorylation, these changes must be due to the absolute amount of NF in the brain after HI and could reflect a change in synthesis or degradation. Table

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