Glial calcium: Homeostasis and signaling function

被引:561
作者
Verkhratsky, A [1 ]
Orkand, RK
Kettenmann, H
机构
[1] Max Delbruck Ctr Mol Med, Dept Cellular Neurosci, Berlin, Germany
[2] Univ Puerto Rico, Inst Neurobiol, San Juan, PR 00901 USA
关键词
D O I
10.1152/physrev.1998.78.1.99
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Glial cells respond to various electrical, mechanical, and chemical stimuli, including neurotransmitters, neuromodulators, and hormones, with an increase in intracellular Ca2+ concentration ([Ca2+](i)). The increases exhibit a variety of temporal and spatial patterns. These [Ca2+](i) responses result from the coordinated activity of a number of molecular cascades responsible for Ca2+ movement into or out of the cytoplasm either by way of the extracellular space or intracellular stores. Transplasmalemmal Ca2+ movements may be controlled by several types of voltage-and ligand-gated Ca2+-permeable channels as well as Ca2+ pumps and a Na+/Ca2+ exchanger. In addition, glial cells express various metabotropic receptors coupled to intracellular Ca2+ stores through the intracellular messenger inositol 1,4,5-trisphosphate. The interplay of different molecular cascades enables the development of agonist-specific patterns of Ca2+ responses. Such agonist specificity may provide a means for intracellular and intercellular information coding. Calcium signals can traverse gal, junctions between glial cells without decrement. These waves can serve as a substrate for integration of glial activity. By controlling gap junction conductance, Ca2+ waves may define the limits of functional glial networks. Neuronal activity can trigger [Ca2+](i) signals in apposed glial cells, and moreover, there is some evidence that glial [Ca2+](i) waves can affect neurons. Glial Ca2+ signaling can be regarded as a form of glial excitability.
引用
收藏
页码:99 / 141
页数:43
相关论文
共 465 条
[31]   GABA-ACTIVATED AND GLUTAMATE-ACTIVATED CURRENTS IN GLIAL-CELLS OF THE MOUSE CORPUS-CALLOSUM SLICE [J].
BERGER, T ;
WALZ, W ;
SCHNITZER, J ;
KETTENMANN, H .
JOURNAL OF NEUROSCIENCE RESEARCH, 1992, 31 (01) :21-27
[32]   SODIUM AND CALCIUM CURRENTS IN GLIAL-CELLS OF THE MOUSE CORPUS-CALLOSUM SLICE [J].
BERGER, T ;
SCHNITZER, J ;
ORKAND, PM ;
KETTENMANN, H .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1992, 4 (12) :1271-1284
[33]  
Bernstein M, 1996, J NEUROSCI RES, V46, P152, DOI 10.1002/(SICI)1097-4547(19961015)46:2<152::AID-JNR3>3.0.CO
[34]  
2-G
[35]   INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING [J].
BERRIDGE, MJ .
NATURE, 1993, 361 (6410) :315-325
[36]   CAPACITATIVE CALCIUM-ENTRY [J].
BERRIDGE, MJ .
BIOCHEMICAL JOURNAL, 1995, 312 :1-11
[37]   CYTOSOLIC CALCIUM OSCILLATORS [J].
BERRIDGE, MJ ;
GALIONE, A .
FASEB JOURNAL, 1988, 2 (15) :3074-3082
[38]   THE PRESENCE OF VOLTAGE-GATED SODIUM, POTASSIUM AND CHLORIDE CHANNELS IN RAT CULTURED ASTROCYTES [J].
BEVAN, S ;
CHIU, SY ;
GRAY, PTA ;
RITCHIE, JM .
PROCEEDINGS OF THE ROYAL SOCIETY SERIES B-BIOLOGICAL SCIENCES, 1985, 225 (1240) :299-313
[39]   PLATELET-ACTIVATING-FACTOR (PAF) RECEPTOR IN RAT-BRAIN - PAF MOBILIZES INTRACELLULAR CA2+ IN HIPPOCAMPAL-NEURONS [J].
BITO, H ;
NAKAMURA, M ;
HONDA, Z ;
IZUMI, T ;
IWATSUBO, T ;
SEYAMA, Y ;
OGURA, A ;
KUDO, Y ;
SHIMIZU, T .
NEURON, 1992, 9 (02) :285-294
[40]   CLONING, EXPRESSION AND TISSUE DISTRIBUTION OF RAT PLATELET-ACTIVATING-FACTOR-RECEPTOR CDNA [J].
BITO, H ;
HONDA, Z ;
NAKAMURA, M ;
SHIMIZU, T .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1994, 221 (01) :211-218