TEMPORAL AND EGIONAL PROFILES OF CYTOSKELETAL PROTEIN ACCUMULATION INTHE RAT-BRAIN FOLLOWING TRAUMATIC BRAIN INJURY

To characterize the cytoskeletal aberration due to traumatic injury, t emporal and regional profiles of changes in immunoreactivity of microt ubule-associated protein 2 (MAP2), neurofilament heavy subunit protein (NFH) and heat shock protein 72 (HSP72) were investigated after diffe rent magnitudes of traumatic brain injury by fluid percussion. The exp erimental rat brain was perfusion-fixed at 1, 6 and 24 hours after tra umatic brain injury. Conventional histological staining has demonstrat ed that the mildest traumatic brain injury (1.0 atm) induced no neuron al loss at the impact site and that neuron loss was apparent when trau matic brain injury was increased to 4.3 arm. The mildest traumatic bra in injury, however, caused a significant increase in HSP72 immunoreact ivity in the superficial cortical layers at the impact site as early a s 1 hour after the injury. In the case of severe traumatic brain injur y (4.3 atm), neuron loss was apparent in the area at the impact site, but the increase in HSP72 immunoreactivity was moderate, and it was ob served only after 6 hours in the deep cortical layers under the necrot ic area. The increased immunostaining of MAP2 was demonstrated in dama ged axons and neuronal perikarya in the wider area surrounding the imp act site at 6 and 24 hours after the injury. Six and 24 hows after the injury, perikaryal accumulation of neurofilament was observed, and th e accumulated neurofilament was mostly phosphorylated. These results i ndicate that the severe traumatic brain injury of 4.3 atm triggers the abnormal accumulation of cytoskeletal proteins in neuronal perikarya, most probably due to an impairment of axonal transport. It is implied that the increased expression of HSP72 may be involved in the protect ive process of neurons after traumatic brain injury.