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Store-operated Ca2+ entry-dependent Ca2+ refilling in the endoplasmic reticulum in astrocytes.

Authors
  • Okubo, Yohei1
  • Iino, Masamitsu2
  • Hirose, Kenzo3
  • 1 Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 133-0033, Japan. Electronic address: [email protected] , (Japan)
  • 2 Division of Cellular and Molecular Pharmacology, Nihon University School of Medicine, 30-1 Oyaguchi Kamicho, Itabashi-ku, Tokyo, 173-8610, Japan. , (Japan)
  • 3 Department of Pharmacology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 133-0033, Japan. , (Japan)
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier
Publication Date
Dec 04, 2019
Identifiers
DOI: 10.1016/j.bbrc.2019.12.006
PMID: 31812243
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Astrocytes regulate various brain functions, for which Ca2+ release from the endoplasmic reticulum (ER) often play crucial roles. Because astrocytic ER Ca2+ release is robust and frequent, the ER Ca2+ refilling mechanism should be critical for ongoing Ca2+ signaling in astrocytes. In this study, we focused on the putative functional significance of store-operated Ca2+ entry (SOCE) in ER Ca2+ refilling. We expressed the ER luminal Ca2+ indicator G-CEPIA1er in astrocytes in acute cortical slices to directly monitor the decrease and recovery of ER Ca2+ concentration upon spontaneous or norepinephrine-induced Ca2+ release. Inhibition of SOCE significantly slowed the recovery of ER Ca2+ concentration after Ca2+ release in astrocytes. This delayed recovery resulted in a prolonged decrease in the ER Ca2+ content in astrocytes with periodic spontaneous Ca2+ release, followed by the attenuation of cytosolic Ca2+ responses upon Ca2+ release. Therefore, our results provide direct evidence for the physiological significance of SOCE in ER Ca2+ refilling after ER Ca2+ release. Copyright © 2019 Elsevier Inc. All rights reserved.

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