کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3055562 1580186 2013 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Metabolic injury to axons and myelin
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی عصب شناسی
پیش نمایش صفحه اول مقاله
Metabolic injury to axons and myelin
چکیده انگلیسی

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 Ca2 + 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. Ca2 + influx) and transmitter release; together these events further promote more Ca2 + influx, while at the same time triggering even more toxic Ca2 + release from intracellular Ca2 + stores. Uncontrolled intracellular Ca2 + increases overactivate a variety of Ca2 +-sensitive enzyme systems culminating in permanent injury to axon, myelin and glia.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 246, August 2013, Pages 26–34
نویسندگان
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