期刊
NATURE NEUROSCIENCE
卷 18, 期 5, 页码 708-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.4001
关键词
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资金
- US National Institutes of Health (NIH) [NS060677]
- NIH [MH099559A, MH104069, MH101198-1]
- CHDI Foundation
- Simon's Foundation Circuits Grant
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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