Ca2+ signaling in astrocytes from Ip3r2−/− mice in brain slices and during startle responses in vivo
Intracellular Ca2+ signaling is considered to be important for multiple astrocyte functions in neural circuits. However, mice devoid of inositol triphosphate type 2 receptors (IP3R2) reportedly lack all astrocyte Ca2+ signaling, but display no neuronal or neurovascular deficits, implying that astroc...
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Published in: | Nature neuroscience 2015-04, Vol.18 (5), p.708-717 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | eng |
Subjects: | |
Online Access: | Get full text |
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Summary: | Intracellular Ca2+ signaling is considered to be important for multiple astrocyte functions in neural circuits. However, mice devoid of inositol triphosphate type 2 receptors (IP3R2) reportedly lack all astrocyte Ca2+ signaling, but display no neuronal or neurovascular deficits, implying that astrocyte Ca2+ fluctuations are not involved in these functions. An assumption has been that the loss of somatic Ca2+ fluctuations also reflects a similar loss in astrocyte processes. We tested this assumption and found diverse types of Ca2+ fluctuations in astrocytes, with most occurring in processes rather than in somata. These fluctuations were preserved in Ip3r2-/- (also known as Itpr2-/- ) mice in brain slices and in vivo, occurred in end feet, and were increased by G protein-coupled receptor activation and by startle-induced neuromodulatory responses. Our data reveal previously unknown Ca2+ fluctuations in astrocytes and highlight limitations of studies that used Ip3r2-/- mice to evaluate astrocyte contributions to neural circuit function and mouse behavior. |
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ISSN: | 1097-6256 1546-1726 |