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胶质细胞功能障碍是缺血半暗带神经元死亡的初始原因吗?

Is glia disfunction the initial cause of neuronal death in ischemic penumbra?

作者信息

Largo C, Cuevas P, Herreras O

机构信息

Servicio de Neurobiologia, Hospital Ramón y Cajal, Madrid, Spain.

出版信息

Neurol Res. 1996 Oct;18(5):445-8. doi: 10.1080/01616412.1996.11740449.

DOI:10.1080/01616412.1996.11740449
PMID:8916059
Abstract

The supportive role of glial cells on neuronal function and survival has been studied in anesthetized rats by using the selective gliotoxin fluorocitrate. Disabling glia operation reproduced many features of ischemic penumbra. An initial mild acidosis and increased interstitial potassium but not glutamate was followed after 3-4 h by repetitive spreading depression waves. These gradually provoked higher levels of acidosis, potassium and glutamate, gradual neuronal function decay and finally, neuron death. We conclude that neurons become highly vulnerable to spreading depression waves only in absence of normal glia operation. Our findings directly associate early glial disfunction to neuronal loss and lead to new insights for the understanding of ischemic pathology.

摘要

通过使用选择性胶质细胞毒素氟柠檬酸,在麻醉大鼠中研究了胶质细胞对神经元功能和存活的支持作用。使胶质细胞失活的操作重现了缺血半暗带的许多特征。最初出现轻度酸中毒和细胞外钾离子增加,但谷氨酸未增加,3-4小时后出现反复的扩散性抑制波。这些逐渐引发更高水平的酸中毒、钾离子和谷氨酸,导致神经元功能逐渐衰退,最终导致神经元死亡。我们得出结论,只有在缺乏正常胶质细胞功能的情况下,神经元才会对扩散性抑制波高度敏感。我们的研究结果直接将早期胶质细胞功能障碍与神经元丢失联系起来,并为理解缺血性病理学带来了新的见解。

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