Inhibition of Calpain Mediated Proteolytic Damage

As noted earlier in this chapter, disruption of intracellular Ca2 + homeostasis is a critical issue in the secondary neurodegenerative pathophysiology of stroke, TBI, and SCI. Following an injurious event, there is a massive posttraumatic Ca2 + influx, initially caused by depolarization-induced glutamate release and the opening of glutamate receptor-operated and voltage-dependent Ca2 + channels.3,4 Increased intracellular Ca2 + concentrations in TBI models have been demonstrated in each of the mainstream rodent TBI models.5 Excessive intracellular Ca2 +

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