Abstract
Ischemia kills neurons not only by direct energy deprivation or membrane disruption during the acute phase, but also initiates a time-related series of extracellular and intra-neuronal events that lead to delayed selective degeneration of vulnerable neurons in certain brain regions. Unfortunately, the sequence of events between the ischemic episode and delayed neuronal death is not completely clear. One of the best documented hypotheses concerning the pathogenesis of ischemic neuronal degeneration is that sustained elevation of intracellular calcium triggers a variety of intracellular events that, if left uncontrolled, can lead to pathologic changes in susceptible neurons (1).
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Zalewska, T., Zablocka, B., Saido, T.C., Domañska-Janik, K. (1997). On the Mechanism of Calpain Activation Under Ischemia. In: Teelken, A., Korf, J. (eds) Neurochemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5405-9_68
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DOI: https://doi.org/10.1007/978-1-4615-5405-9_68
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