title: Ca(2+) signaling in astrocytes from Ip3r2(-/-) mice in brain slices and during startle responses in vivo.
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.
authors.affiliation: Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
authors.forename: Rahul
authors.initials: R
authors.lastname: Srinivasan
authors.affiliation: Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
authors.forename: Ben S
authors.initials: BS
authors.lastname: Huang
authors.affiliation: Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
authors.forename: Sharmila
authors.initials: S
authors.lastname: Venugopal
authors.affiliation: Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
authors.forename: April D
authors.initials: AD
authors.lastname: Johnston
authors.affiliation: Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
authors.forename: Hua
authors.initials: H
authors.lastname: Chai
authors.affiliation: Allen Institute for Brain Science, Seattle, Washington, USA.
authors.forename: Hongkui
authors.initials: H
authors.lastname: Zeng
authors.affiliation: 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.
authors.forename: Peyman
authors.initials: P
authors.lastname: Golshani
authors.affiliation: 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.
authors.forename: Baljit S
authors.initials: BS
authors.lastname: Khakh
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000502:physiology* / Q000648:ultrastructure; D020013:Calcium Signaling / Q000502:physiology*; D003433:Crosses, Genetic; D005260:Female; D005456:Fluorescent Dyes; D006624:Hippocampus / Q000166:cytology / Q000502:physiology; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000172:deficiency* / Q000235:genetics; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D011224:Prazosin / Q000494:pharmacology; D013216:Reflex, Startle / Q000187:drug effects / Q000502:physiology*; D012984:Software
chemical_list: D005456:Fluorescent Dyes; D053496:Inositol 1,4,5-Trisphosphate Receptors; C580990:Ip3r2 protein, mouse; D011224:Prazosin