The roles of calcium in ischaemic brain injury
Bailliere's Clinical Anaesthesiology
The rapid and extensive elevation of intracellular Ca2+ that occurs during even brief interruptions of cerebral blood flow is a key factor contributing to the unique sensitivity of the brain to irreversible ischaemic injury. Abnormal [Ca2+](i) contributes to delayed neuronal death in at least six different ways including degradation of membrane lipids, proteolysis of structural proteins and enzymes, altered gene expression that may induce apoptosis, disruption of mitochondrial energy transduction, potentiation of oxidative stress through stimulation of the production of superoxide and nitric oxide and interneuronal dissemination of potentially toxic signals through stimulation of the release of neurotransmitters including the excito-toxic neurotransmitter glutamate and other neurotransmitters, for example catecholamines. As the activity of receptor-operated and voltage-dependent Ca2+ channels can change following cerebral ischaemia, the releasability of neurotransmitters can be enhanced for many hours following the initial ischaemic period. Altered Ca2+-dependent neurotransmitter release processes are potentially highly consequential factors in the pathogenesis of ischaemic brain injury that should be taken into account in the search for clinically feasible neuroprotective treatment strategies.
Werling, L., & Fiskum, G. (1996). The roles of calcium in ischaemic brain injury. Bailliere's Clinical Anaesthesiology, 10 (3). http://dx.doi.org/10.1016/S0950-3501(96)80028-6