scholarly journals Inositol 1,4,5-trisphosphate receptor type 2-independent Ca2+ release from the endoplasmic reticulum in astrocytes

Glia ◽  
2018 ◽  
Vol 67 (1) ◽  
pp. 113-124 ◽  
Author(s):  
Yohei Okubo ◽  
Kazunori Kanemaru ◽  
Junji Suzuki ◽  
Kenta Kobayashi ◽  
Kenzo Hirose ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Receptor Type ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

539 Inositol 1,4,5-Trisphosphate Receptor Type 2 Modulates Bsep Activity in Hepatocytes

2010 ◽  
Vol 138 (5) ◽  
pp. S-791
Author(s):  
Emma A. Kruglov ◽  
Samir Gautam ◽  
Michael H. Nathanson
Keyword(s):  
Receptor Type ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

Up-regulation of inositol 1,4,5-trisphosphate receptor type 1 is responsible for a decreased endoplasmic-reticulum Ca2+ content in presenilin double knock-out cells

Cell Calcium ◽  
2006 ◽  
Vol 40 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Nael Nadif Kasri ◽  
Sarah L. Kocks ◽  
Leen Verbert ◽  
Sébastien S. Hébert ◽  
Geert Callewaert ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Receptor Type ◽  
Knock Out ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

scholarly journals Inositol 1,4,5-trisphosphate receptor type2-independent Ca2+ release from the endoplasmic reticulum in astrocytes

2018 ◽  
Author(s):  
Yohei Okubo ◽  
Kazunori Kanemaru ◽  
Junji Suzuki ◽  
Kenta Kobayashi ◽  
Kenzo Hirose ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Close Contact ◽  
Functional Deficits ◽  
Highly Sensitive ◽  
Close Proximity ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Ca ◽  
Hippocampal Astrocytes ◽  
Trisphosphate Receptor

AbstractAccumulating evidence indicates that astrocytes are actively involved in the physiological and pathophysiological functions of the brain. Intracellular Ca2+ signaling, especially Ca2+ release from the endoplasmic reticulum (ER), is considered to be crucial for the regulation of astrocytic functions. Mice with genetic deletion of inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) are reportedly devoid of astrocytic Ca2+ signaling, and thus widely used to explore the roles of Ca2+ signaling in astrocytic functions. While functional deficits in IP3R2-knockout (KO) mice have been found in some reports, no functional deficit was observed in others. Thus, there remains a controversy regarding the functional significance of astrocytic Ca2+ signaling. To address this controversy, we re-evaluated the assumption that Ca2+ release from the ER is abolished in IP3R2-KO astrocytes using a highly sensitive imaging technique. We expressed the ER luminal Ca2+ indicator G-CEPIA1er in cortical and hippocampal astrocytes to directly visualize spontaneous and stimulus-induced Ca2+ release from the ER. We found attenuated but significant Ca2+ release in response to application of norepinephrine to IP3R2-KO astrocytes. This IP3R2-independent Ca2+ release induced only minimal cytosolic Ca2+ transients but induced robust Ca2+ increases in mitochondria that are frequently in close contact with the ER. These results indicate that ER Ca2+ release is retained and is sufficient to increase the Ca2+ concentration in close proximity to the ER in IP3R2-KO astrocytes.

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