Metabolic injury to axons and myelin

Experimental Neurology
Shigeki Tsutsui, P K Stys

Abstract

CNS white matter, the collection of axons and supporting glia of the mammalian CNS, makes up close to 50% of the human brain by volume. Interruption of vital interconnects within this tissue, even over a short segment, often leads to serious morbidity in a broad range of neurological disorders. Axons, glia and myelin express a complex array of conventional voltage gated ion channels, intracellular Ca(2+) release channels, neurotransmitter uptake and release mechanisms, together with matching transmitter receptors. Dysregulation of ion homeostasis induced by injury or energy failure leads to depolarization and intracellular Na(+) accumulation, which in turn triggers inappropriate ion translocation (i.e. Ca(2+) influx) and transmitter release; together these events further promote more Ca(2+) influx, while at the same time triggering even more toxic Ca(2+) release from intracellular Ca(2+) stores. Uncontrolled intracellular Ca(2+) increases overactivate a variety of Ca(2+)-sensitive enzyme systems culminating in permanent injury to axon, myelin and glia.

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Citations

Jan 25, 2013·Molecular Neurobiology·Nian Cao, Zhong-Xiang Yao
Aug 31, 2012·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Anna G BarsukovaDennis Bourdette
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