Calpain, a Catabolic Mediator in Spinal Cord Trauma
Spinal cord trauma causes tissue damage and necrosis with neurological dysfunction proportional to the severity of injury. The traumatic morphology in the cord lesion correlates with the extent of the neurochemical alterations. The changes include axonal granular degeneration, myelin vesiculation and phagocytosis, losses of axonal and myelin protein and lipids and an accumulation of calcium. Subsequently, there is an increased activity of lysosomal and neutral proteinase in the lesion with the greatest change an elevated activity of neutral proteinase. Although no single factor has been implicated in the pathogenesis of secondary injury, calcium is clearly one of the most important players in spinal cord injury tissue degeneration. Calcium plays many roles in cell function; an important one being enzyme activation of both proteinase and lipase. Lipase activation releases arachidonic acid and initiates a cascade of reactions that are also observed following vascular injury. Calcium also activates the neutral proteinase, calpain, which degrades endogenous substrate cytoskeletal and myelin protein and is associated with neuronal death, axonal degeneration and myelinolysis. This tightly linked series of events suggest a pivotal role for calpain in the tissue destruction of spinal cord trauma. This short chapter deals with the importance of calpain as a catabolic mediator in spinal cord injury. This may serve as a model for events occurring in other brain degenerative disorders.
KeywordsSpinal Cord Injury Myelin Protein Neutral Proteinase Calpain Activity Spinal Cord Trauma
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