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Publication : Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo.

First Author  Srinivasan R Year  2015
Journal  Nat Neurosci Volume  18
Issue  5 Pages  708-17
PubMed ID  25894291 Mgi Jnum  J:222858
Mgi Id  MGI:5645832 Doi  10.1038/nn.4001
Citation  Srinivasan R, et al. (2015) Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo. Nat Neurosci 18(5):708-17
abstractText  Intracellular Ca(2+) 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 Ca(2+) signaling, but display no neuronal or neurovascular deficits, implying that astrocyte Ca(2+) fluctuations are not involved in these functions. An assumption has been that the loss of somatic Ca(2+) fluctuations also reflects a similar loss in astrocyte processes. We tested this assumption and found diverse types of Ca(2+) 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 Ca(2+) 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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