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Glutamate receptors and white matter stroke

机译:谷氨酸受体和白质中风

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摘要

White matter (WM) damage during ischemia occurs at multiple sites including myelin, oligodendrocytes, astrocytes and axons. A major driver of WM demise is excitoxicity as a consequence of excessive glutamate release by vesicular and non-vesicular mechanisms from axons and glial cells. This results in over-activation of ionotropic glutamate receptors (GluRs) profusely expressed by all cell compartments in WM. Thus, blocking excitotoxicity in WM with selective antagonists of those receptors has a potential therapeutic value. The significance of WM GluR expression for WM stroke injury is the focus of this review, and we will examine the role of GluRs in injury to myelin, oligodendrocytes, astrocytes and the axon cylinder.
机译:在缺血期间发生白质(WM)损伤发生在包括髓鞘,少霉素,星形胶质细胞和轴突的多个位点。 WM Demise的主要驱动器是兴奋毒性,作为通过来自轴突和胶质细胞的囊泡和非凹形机制过度谷氨酸释放的结果。 这导致通过Wm中的所有细胞隔间对离子胶质谷氨酸受体(Glower)的过度激活。 因此,用那些受体的选择性拮抗剂阻断WM中的兴奋毒性具有潜在的治疗价值。 WM Glus表达对WM中风损伤的重要性是本综述的重点,我们将研究Glars在髓鞘损伤中的作用,少霉素,星形胶质细胞和轴突缸。

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