Mehmet Demirci

Despite the clinical importance, little is known about the mechanisms of ischemic injury in white matter. Studies over the past few years showed that early anoxic injury in white matter depends on the presence of extracellular Ca²⁺ and myelination. An increase in [ Na^+] _i due to anoxic depolarization causes reverse operation of the Na⁺-Ca²⁺ exchanger, which mediates Ca²⁺ influx during anoxia. The resistance of premyelinated and amyelinated axons to anoxic injury supports the hypothesis that Ca²⁺ influx occurs at nodes of Ranvier in axons. It is not known what cascades of events are triggered by Ca²⁺ influx in white matter, and whether anoxia induces increases in intracellular Ca²⁺ in also glial cells.