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Nat Neurosci. 2015 May;18(5):708-17. doi: 10.1038/nn.4001. Epub 2015 Apr 20.

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

Author information

1
Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
2
Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
3
Allen Institute for Brain Science, Seattle, Washington, USA.
4
1] Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [2] Integrative Center for Learning and Memory, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [3] West Los Angeles VA Medical Center, Los Angeles, California, USA.
5
1] Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [2] Department of Neurobiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.

Abstract

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.

PMID:
25894291
PMCID:
PMC4429056
DOI:
10.1038/nn.4001
[Indexed for MEDLINE]
Free PMC Article

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