Calcium and glial cell death

被引：60

作者：

Alberdi, E ^{[1
]}

Sánchez-Gómez, MV ^{[1
]}

Matute, C ^{[1
]}

机构：

[1] Univ Basque Country, Fac Med & Odontol, Dept Neurociencias, Leioa 48940, Spain

来源：

CELL CALCIUM | 2005年 / 38卷 / 3-4期

关键词：

isquemia; excitotoxicity; mitochondria; reactive oxygen species; apoptosis; degeneration;

D O I：

10.1016/j.ceca.2005.06.020

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Calcium (Ca2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca2+-permeable receptors and channels, as well as store-operated channels and pumps, all of which determine Ca2+ homeostasis. In addition, glial cells detect functional activity in neighbouring neurons and respond to it by means of Ca2+ signals that can modulate synaptic interactions. Like in neurons, Ca2+ overload resulting from dysregulation of channels and pumps can be deleterious to glia. In this review, we summarize recent advances in the understanding Ca2+ homeostasis in glial cells, the consequences of its alteration in cell demise as well as in neurological and psychiatric disorders that experience glial cell loss. (C) 2005 Elsevier Ltd. All rights reserved.

引用

页码：417 / 425

页数：9

共 78 条

[1] Ca2+ influx through AMPA or kainate receptors alone is sufficient to initiate excitotoxicity in cultured oligodendrocytes [J].