Enzyme histochemical changes after transection or hemisection of the spinal cord of the rat

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The spinal cords of 84 young adult female rats were transected or hemisected at T7 to T8 and the animals autopsied at intervals from 6 h to 14 months postoperatively. Frozen sections of the unfixed spinal cord on either side of the lesion were prepared for enzyme histochemistry, immunocytochemistry, and histology. The most striking enzymatic alterations and their physiological implications were: (i) (Na +K +)-activated ATPase activity decreased in axons of the gray and white matter within 6 h after spinal transection and did not return subsequently, whereas the decrease in activity that occurred contralateral to a hemisection was transient. The decreased activity occurred so promptly as to suggest possible roles in the genesis of the initial flaccid paralysis (spinal shock) in the spinal animal and in the temporary paraplegia seen after subtotal spinal injury. (ii) During the first week postoperatively, many axons in the white matter developed large swellings or small varicosities that reacted strongly only for enzymes normally present in the neuronal perikaryon (e.g., AChE, acid phosphatase, NADH-diaphorase, and G6PDH). This histopathological reaction gradually spread rostrally and caudally from the site of injury, but it disappeared as axonal degeneration supervened. (iii) Within 7 days after spinal transection, many neuronal perikarya were chromatolytic and exhibited decreased AChE activity but normal or increased NADH-diaphorase activity. This response is similar to that seen in the cell bodies of regenerating peripheral axons where anabolic processes are favored over neurotransmission-related functions. (iv) Increased cellularity of the spinal parenchyma adjacent to the lesion resulted largely from the proliferation and hypertrophy of astrocytes. These hypertrophied cells, whose identity was confirmed by GFAP immunocytochemistry, reacted with marked intensity for NADH-diaphorase, G6PDH, and Gly3PDH. Such enzyme changes, characteristic of increased protein turnover, indicate that experimental attempts to control gliosis (e.g., by reducing protein turnover or by other means) could be effectively monitored by enzyme histochemistry.