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Our understanding of calcium's role in cerebral ischemia continues to evolve from the initial recognition that it may be harmful to the ischemic cell. A multitude of experiments have supported the hypothesis that excessive influx of calcium into the cell under ischemic conditions is a major mechanism of cell injury and death. Pharmacological intervention to restore cellular calcium homeostasis is protective in many models of cell anoxia. Principle routes of calcium entry are the voltage-sensitive (VSCC) and N-methyl-D-aspartate linked receptor operated (ROCC) calcium channels. Regional variations in channel densities have been described and it is now known that these classes of channels are located in different regions of the neurons. Activation of both channel types has been identified in in vivo models of cerebral ischemia. Although the ROCC is predominant in number, the VSCC appears to activate at higher cerebral blood flow values suggesting that it is an earlier conduit for calcium than the glutamate-driven ROCC. Intracellular calcium is well recognized as a second messenger system and there is increasing appreciation that it induces immediate early genes (IEG). Since IEGs function as transcriptional regulating factors, the differential expression of specific target genes may be of importance for determining death or survival of the ischemic tissue.
Morley et al. (Sat,) studied this question.