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Glial calcium: Homeostasis and signaling function

Item Type:Review
Title:Glial calcium: Homeostasis and signaling function
Creators Name:Verkhratsky, A. and Orkand, R.K. and Kettenmann, H.
Abstract: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 Ca(2+)-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-triphosphate. 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 gap 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.
Keywords:Brain, Calcium, Calcium Channels, Homeostasis, Neuroglia, Neurotransmitter Agents, Organelles, Signal Transduction, Animals
Source:Physiological Reviews
ISSN:0031-9333
Publisher:American Physiological Society (U.S.A.)
Volume:78
Number:1
Page Range:99-141
Date:January 1998
Official Publication:http://physrev.physiology.org/cgi/content/abstract/78/1/99
PubMed:View item in PubMed

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