Abstract
Calcium ions (Ca2+) are ubiquitous second messengers that play an important role in many physiological events including secretion, development, fertilization, and gene expression. However, the proper spatio-temporal regulation of the intracellular Ca2+ concentration is necessary to fulfill the function, and disturbed Ca2+ signaling is known to cause cell death and pathological disease. Inositol 1, 4, 5-trisphosphate receptor (IP3R) is a Ca2+ channel localized on the endoplasmic reticulum (ER) in the many types of cells including neurons, and is a key player to generate the proper intracellular Ca2+ dynamics for cell function. Disruption of IP3Rs leads to various physiological defects including neural development and neural plasticity. Moreover, several lines of evidence indicate that the altered IP3R activity causes supranormal Ca2+ homeostasis leading to various pathological diseases. In this review, we describe how IP3R activity is properly regulated by myriads of associated proteins, and discuss the physiological role of IP3Rs especially in neurons.
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Abbreviations
- CTD:
-
C-terminal domain
- HAP1A:
-
Htt-associated protein-1A
- Htt:
-
Huntingtin
- IP3R:
-
Inositol 1, 4, 5-trisphosphate receptor
- LFS:
-
low-frequency stimulation
- LTD:
-
long-term depression
- LTP:
-
long-term potentiation
- MSNs:
-
medium spiny neurons
- NMDA:
-
N-methyl-d-aspartate
- PTP:
-
permeability transient pore
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Acknowledgement
We thank Dr. Akihiro Mizutani and Dr. Yukiko Kuroda for fruitful comments on the manuscript. Supported by grants from the Ministry of Education, Science, and Culture of Japan (K. M. and Y. N.), Grant-in-Aid for Young Scientists (C. H.), and the Japan Science and Technology Agency.
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Hisatsune, C., Mikoshiba, K. (2009). IP3 Receptor and Ca2+ Signaling. In: Lajtha, A., Mikoshiba, K. (eds) Handbook of Neurochemistry and Molecular Neurobiology. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-30370-3_31
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