Intracellular Calcium Accumulation

During ischemia, the cytosolic concentration of calcium can increase as much as 1000-fold. Intracellular calcium levels rise via several mechanisms. Calcium influx occurs during cerebral ischemia as a result of the fall in adenosine triphosphate (ATP) levels and membrane depolarization (6), leading to VDCC opening and reversal of the Na+ - Ca2+ exchanger (7). Increased release of the EAA glutamate also occurs after ischemia and, by stimulation of glutamate receptors, leads to calcium influx by opening appropriate ion channels. Mitochondria are important sources of intracellular calcium accumulation. Approximately 50% of intra-cellular calcium is normally stored in the mitochondria and is released under conditions of acidosis and energy depletion. Calcium stored in the ER is released into the cytosol through ischemia-induced activation of phospholipase C (8). Low calcium levels in the ER could impair normal protein folding and processing, leading to ER stress, which in turn, activates the unfolded protein response, involving the activation of 2 kinases that phosphorylate eukaryotic initiation factor 2a, resulting in its inactivation and the shutdown of protein synthesis (9,10).

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