Alberdi Elena, Sánchez-Gómez María Victoria, Matute Carlos
Departamento de Neurociencias, Facultad de Medicina y Odontología. Universidad del País Vasco, 48940 Leioa, Spain.
Cell Calcium. 2005 Sep-Oct;38(3-4):417-25. doi: 10.1016/j.ceca.2005.06.020.
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.
钙（Ca2+）稳态对于包括中枢神经系统（CNS）神经胶质细胞在内的几乎所有类型细胞的发育和存活都至关重要。星形胶质细胞、少突胶质细胞和小胶质细胞是中枢神经系统中的主要胶质细胞类型，它们拥有一系列相当复杂的Ca2+通透受体和通道，以及储存-操纵通道和泵，所有这些都决定了Ca2+稳态。此外，神经胶质细胞检测相邻神经元的功能活动，并通过可调节突触相互作用的Ca2+信号对其作出反应。与神经元一样，通道和泵调节异常导致的Ca2+超载对神经胶质细胞可能是有害的。在这篇综述中，我们总结了在理解神经胶质细胞Ca2+稳态方面的最新进展，其改变在细胞死亡以及经历神经胶质细胞丢失的神经和精神疾病中的后果。
