Abstract
Intracellular Ca2+ overload, excitotoxic activity of glutamate and concomitant generation of free radicals are thought to play the prominent role as triggering factors in the pathogenesis of brain ischemic-reperfusion injury (IRI) (1). While calcium acts as an important second messenger in the regulation of various neural activities (2), it also acts as an essential mediator of neuronal cell damage in IRI by stimulating of Ca2+ -dependent degradative processes and disaggregation of cytoskeletal components (3). Post-ischemic accumulation of Ca2+ is thought to be responsible for delayed neuronal death of selective regions of hippocampus, but it is not yet clear which sources of Ca2+ and which pathways are involved (4).
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Lehotský, J., Kaplan, P., Raçay, P., Raeymaekers, L., Mézešová, V. (1997). Ischemia-Reperfusion Decreases Protein Levels of InsP3 Receptor and PMCA but not Organellar Ca2+ Pump and Calreticulin in Gerbil Forebrain. In: Teelken, A., Korf, J. (eds) Neurochemistry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5405-9_63
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DOI: https://doi.org/10.1007/978-1-4615-5405-9_63
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