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Cerebral Protection. Part I

The increased understanding of the pathogenesis of ischemic neuronal damege has opened new approaches in research for improving protective methods through the addition of appropriate pharmacological agents.The failure of neurotrasmitter transport is an essential step in the pathogenesis of ischemic cerebral injury. Ater release into the intercellular space, glutamate is taken up into glial cells and rapidly converted to glutamine after which it reenters the neuron ready to be used for the next message. Under conditions of hypoxia or ischemia, the conversion of glutamate to glutamine is interrupted. This leads to its accumulatioon in the intercellular space, where glutamate acts as a neurotoxic substance. Here its opens calcium channels, leading to an influx of calcium, which then initiates the catastrophic intracellular cascade leding to neuronal apoptosis and cell death.  (Lipton and Rosenberg 1995).