IPR1-dependent astrocyte calcium signaling in chronic itch.

Miho Shiratori-Hayashi, Makoto Tsuda

Journal: Neuroscience research 2023;187():40-44

PMID: 36181909

Abstract

Astrocytes, the most abundant type of glial cell, are electrically non-excitable cells that use intracellular calcium (Ca) for functional regulation. Changes in intracellular Ca concentration play important roles in the central nervous system (CNS), as they are involved in the release of gliotransmitters and the control of extracellular ion concentrations, thereby affecting the regulation of neuronal excitability, CNS homeostasis, and behavior. Intracellular calcium mobilization in astrocytes is known to be mediated via inositol 1,4,5-trisphosphate receptors (IPRs), particularly IPR2, and its association with CNS pathogenesis has been widely reported. In addition, the existence of IPR2-independent calcium signaling has recently been postulated; however, the detailed mechanisms and its role in astrocyte functions and CNS pathogenesis are still poorly understood. In this paper, we describe the putative mechanisms underlying IPR1-dependent calcium signaling in astrocytes and its effects on the reactive state, compare this signaling with IPR2-dependent calcium signaling, and discuss its contribution to chronic itch-like behavior.

Copyright © 2022. Published by Elsevier B.V.

Address: Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan. Electronic address: [email protected].; Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan; Kyushu University Institute for Advanced Study, Fukuoka, Japan. Electronic address: [email protected].

Link outs

Subscription / membership required

Bant logo

© Copyright 2026, Nutrition Evidence

NED wishes to thank the following organisations for their support:

We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.