Excitotoxicity Intracellular Calcium And Ischemic Brain Injury

Energy failure due to cessation of blood flow can result in calcium accumulation in brain cells via diffusion along electrochemical gradients, depolarization and opening of voltage-dependent calcium channels (VDCC), internal release from organelles [the endoplasmic reticulum (ER) and mitochondria], and via excessive stimulation of glutamate receptors. Ischemia also results in the accumulation and release of excitatory amino acids (EAAs), such as glutamate and aspartate, which contribute to neuronal cell death via entry of calcium and sodium ions. Ischemia-induced calcium toxicity can then lead to cytoskeletal breakdown, altered gene expression, lipolysis, and generation of ROS and reactive nitrogen species (RNS) (Fig. 2) (5).

Figure 1 Schematic diagram showing the ischemic penumbra and core. Following occlusion of the middle cerebral artery, CBF decreases to 0 to 12 mL /100 g /min in regions of the most severe injury (core). The peri-infarct area is sometimes termed penumbra, where the CBF is maintained at approximately 12 to 24 mL/100 g/min due to collateral blood flow. It is within this region that brain tissue might be salvageable if blood flow is fully restored or an appropriate cytoprotectant is administered. However, penumbra is a time-dependent concept, as it might shrink if the early blood flow can be restored, or it might be incorporated into the core if ischemia is allowed to persist. Abbreviation: CBF, cerebrospinal fluid.

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