Hypoxic-ischemic injury to the prenatal and perinatal brain is a major contributor to morbidity and mortality to infants, often leading to mental retardation, seizures, and cerebral palsy. The susceptibility of the immature CNS to hypoxia-ischemia is largely dependent on the temporal and regional status of critical developmental processes, as well as on the regulation of cerebral blood flow and metabolism. The molecular and biochemical mechanisms of acute injury to the neonatal brain in experimental rodent and murine models of hypoxic-ischemic and ischemic injury, including disturbances of intracellular homeostasis, role of glutamate receptors, free radicals and transitional ions, as well as the modifying role of gene expression to cell death/survival will be reviewed in this chapter.
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