The link between excitotoxic oligodendroglial death and demyelinating diseases

被引：281

作者：

Matute, C ^{[1
]}

Alberdi, E ^{[1
]}

Domercq, M ^{[1
]}

Pérez-Cerdá, F ^{[1
]}

Pérez-Samartín, A ^{[1
]}

Sánchez-Gómez, MV ^{[1
]}

机构：

[1] Univ Basque Country, Dept Neurociencias, Leioa 48940, Spain

来源：

TRENDS IN NEUROSCIENCES | 2001年 / 24卷 / 04期

关键词：

D O I：

10.1016/S0166-2236(00)01746-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Oligodendrocytes, the myelinating cells of CNS axons, are highly vulnerable to excitotoxic signals mediated by glutamate receptors of the AMPA and kainate classes. Receptors in these cells are commonly activated by glutamate that is released from axons and glial cells. In addition, oligodendrocytes contribute to the control of extracellular glutamate levels by means of their own transporters. However, acute and chronic alterations in glutamate homeostasis can result in overactivation of AM PA and kainate receptors and subsequent excitotoxic oligodendroglial death. Furthermore, demyelinating lesions caused by excitotoxins can be similar to those observed in multiple sclerosis. This, together with the effect of AMPA and kainate receptor antagonists in ameliorating the neurological score of animals with experimental autoimmune encephalomyelitis (an animal model of multiple sclerosis), indicates that oligodendrocyte excitotoxicity could be involved in the pathogenesis of demyelinating disorders.

引用

页码：224 / 230

页数：7

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