Glial calcium and diseases of the nervous system

被引:131
作者
Nedergaard, Maiken [1 ]
Rodriguez, Jose J. [2 ,3 ,4 ]
Verkhratsky, Alexei [2 ,5 ]
机构
[1] Univ Rochester, Med Ctr, Dept Neurosurg, Div Glial Dis & Therapeut,Ctr Translat Neuromed, Rochester, NY 14642 USA
[2] ASCR, Inst Expt Med, Prague 14220 4, Czech Republic
[3] Basque Fdn Sci, IKERBASQUE, Bilbao 48011, Spain
[4] Univ Basque Country, Dept Neurosci, UPV EHU, Leioa 48940, Spain
[5] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England
关键词
Glia; Calcium signalling; Astrocytes; Microglia; Neurodegeneration; Psychiatric disorders; Alzheimer's disease; Parkinson's disease; Dementia; Amyotrophic lateral sclerosis; FIBRILLARY ACIDIC PROTEIN; NEURONAL ENDOPLASMIC-RETICULUM; AMPA RECEPTOR SUBUNITS; HIPPOCAMPAL ASTROCYTES; D-SERINE; INTRACELLULAR CALCIUM; GLUTAMATE RECEPTORS; CORTICAL ASTROCYTES; PREFRONTAL CORTEX; MEMBRANE CURRENTS;
D O I
10.1016/j.ceca.2009.11.010
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The evolution of the central nervous system (CNS) resulted in an appearance of highly specialised neuronal networks optimised for rapid information transfer. In the course of this specialisation neuronal cells lost their metabolic independence and the ability to survive in the absence of homeostatic systems. These homeostatic systems, represented by neuroglia regulate all aspects of CNS function in physiological and pathological conditions. The neurological diseases should be therefore considered as primary gliopathologies, which determine the progression and outcome of neuropathological process. Glial function is intimately regulated by cellular calcium signalling that underlies the specific form of "glial calcium excitability". Glial Ca2+ signals are triggered by activation of multiple receptors, and are primarily driven by Ca2+ release from the endoplasmic reticulum. In this review we summarise the role of glial calcium signalling in various forms of pathological processes including neurological and psychiatric disorders and neurodegeneration. (C) 2009 Published by Elsevier Ltd.
引用
收藏
页码:140 / 149
页数:10
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