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PGE2 Potentiates Orai1-Mediated Calcium Entry Contributing To Peripheral Sensitization by Dongyu Wei; Yixiao Mei; Yannong Dou; Xiaodong Huo; Victoria Whitehead; Huijuan Hu is a Medicine article available to read on EtoBox.

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Peripheral sensitization is one of the primary mechanisms underlying the pathogenesis of chronic pain. However, candidate molecules involved in peripheral sensitization remain unclear. We have shown that store-operated calcium channels (SOCs) are expressed in the dorsal root ganglion (DRG) neurons. Whether SOCs contribute to peripheral sensitization associated with chronic inflammatory pain is elusive. Here we report that global or conditional deletion of Orai1, a major component of SOCs, attenuates CFA-induced pain hypersensitivity. To further establish the role of Orai1 in inflammatory pain, we performed calcium imaging and patch clamp recordings in wild type (WT) and Orai1 knockout (KO) DRG neurons. We found that SOC entry (SOCE) and SOC currents were significantly increased in WT, but not in Orai1 KO DRG neurons from CFA- and carrageenan-injected mice. Interestingly, the Orai1 protein level in L3/4 DRGs was not altered under peripheral inflammatory conditions. To understand how Orai1 is modulated, prostaglandin E2 (PGE2) was used to sensitize DRG neurons. PGE2-induced pain hypersensitivity was significantly reduced in Orai1 KO mice. PGE2-induced potentiation of SOCE and SOC cur

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Author

Dongyu Wei; Yixiao Mei; Yannong Dou; Xiaodong Huo; Victoria Whitehead; Huijuan Hu

Publisher

Elsevier BV

Published

2023

Language

EN

Field

Medicine (Health Sciences)