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Visualization of astrocytic intracellular Ca 2+ mobilization
Author(s) -
Okubo Yohei,
Iino Masamitsu
Publication year - 2019
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp277609
Subject(s) - endoplasmic reticulum , intracellular , microbiology and biotechnology , calcium signaling , mobilization , receptor , chemistry , inositol , neuroscience , signalling , inositol trisphosphate , biophysics , biology , biochemistry , archaeology , history
Astrocytes generate robust intracellular Ca 2+ concentration changes (Ca 2+ signals), which are assumed to regulate astrocytic functions that play crucial roles in the regulation of brain functions. One frequently used strategy for exploring the role of astrocytic Ca 2+ signalling is the use of mice deficient in the type 2 inositol 1,4,5‐trisphosphate receptor (IP 3 R2). These IP 3 R2‐knockout (KO) mice are reportedly devoid of Ca 2+ mobilization from the endoplasmic reticulum (ER) in astrocytes. However, they have shown no functional deficits in several studies, causing a heated debate as to the functional relevance of ER‐mediated Ca 2+ signalling in astrocytes. Recently, the assumption that Ca 2+ mobilization from the ER is absent in IP 3 R2‐KO astrocytes has been re‐evaluated using intraorganellar Ca 2+ imaging techniques. The new results indicated that IP 3 R2‐independent Ca 2+ release may generate Ca 2+ nanodomains around the ER, which may help explain the absence of functional deficits in IP 3 R2‐KO mice.