Neuron-glial interaction during injury and edema of the CNS.

O S Kempski, C Volk
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引用次数: 42

Abstract

During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high extracellular potassium. Glial homeostatic mechanisms are activated to prevent the secondary injury from these mediators. The glial clearance mechanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggests glial swelling to occur together with glutamate uptake or in response to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.

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中枢神经系统损伤和水肿过程中神经元与神经胶质的相互作用。
在中枢神经系统损伤和缺血过程中,介质化合物被释放或激活,引起神经细胞的继发性肿胀和损伤。这些介质是谷氨酸、酸中毒、游离脂肪酸或高细胞外钾。神经胶质稳态机制被激活以防止这些介质的继发性损伤。胶质细胞清除机制已经详细研究了使用体外系统允许胶质细胞环境的密切控制。目前的证据表明,胶质肿胀与谷氨酸摄取或细胞外酸中毒反应一起发生。因此,胶质细胞肿胀与其说是胶质细胞死亡的迹象,不如说是内稳态机制的结果。
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