The effects of spinal cord trauma on myelin.
Experimental spinal cord trauma was produced in rats by dropping a 10-g weight from a height of 30 cm upon exposed spinal cord. The histological lesion consisted of edema, necrosis, and hemorrhage. The fine structure of the early traumatic lesion (4 to 12 hours) included granular dissolution of axons and a characteristic vesiculation of myelin. The predominant ultrastructural features of older lesions (12 to 72 hours) were intra-axonal calcification and lipid-laden macrophages. The yield of myelin and the activity of adenosine 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNP) were reduced by approximately 15% at 4 hours and by 60% at 72 hours. Losses in all myelin proteins were observed, but were most severe and occurred earliest in the basic proteins. The ultrastructural and biochemical alterations observed in this study indicate that proteinase activity is increased and may be partially responsible for the traumatic myelinolysis in experimental spinal cord trauma.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D008297:Male; D009185:Myelin Proteins / Q000378:metabolism*; D009186:Myelin Sheath / Q000648:ultrastructure*; D009336:Necrosis; D009410:Nerve Degeneration; D009413:Nerve Fibers, Myelinated / Q000648:ultrastructure*; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009708:Nucleotidases / Q000378:metabolism; D051381:Rats; D013116:Spinal Cord / Q000473:pathology; D013119:Spinal Cord Injuries / Q000201:enzymology / Q000473:pathology*
D009185:Myelin Proteins; D009419:Nerve Tissue Proteins; D009708:Nucleotidases