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The remodeling of store\u2010operated calcium entry (SOCE) involves the refilling of calcium in the endoplasmic reticulum via STIM1 and Orai1 proteins and is crucial for maintaining neural plasticity and neurotransmitter release. The mechanism underlying SOCE\u2010mediated NP remains largely unknown. In this study, we found SOCE\u2010mediated calcium refilling was significantly higher during neuropathic pain, and the major component Orai1 was specifically co\u2010localized with neuronal markers. Intrathecal injection of SOCE antagonist SKF96365 remarkably alleviated nerve injury\u2010 and formalin\u2010induced pain and suppressed c\u2010Fos expression in response to innocuous mechanical stimulation. RNA sequencing revealed that SKF96365 altered the expression of spinal transcription factors, including Fos, Junb, and Socs3, during neuropathic pain. In order to identify the genes critical for SKF96365\u2010induced effects, we performed weighted gene co\u2010expression network analysis (WGCNA) to identify the genes most correlated with paw withdrawal latency phenotypes. Of the 16 modules, MEsalmon module was the most highly correlated with SKF96365 induced effects. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the enriched genes of MEsalmon module were significantly related to Toll\u2010like receptor signaling, steroid biosynthesis, and chemokine signaling, which may mediate the analgesic effect caused by SKF9636 treatment. Additionally, the SOCE antagonist YM\u201058483 produced similar analgesic effects in nerve injury\u2010 and formalin\u2010induced pain. Our results suggest that manipulation of spinal SOCE signaling might be a promising target for pain relief by regulating neurotransmitter production and spinal transcription factor expression.<\/jats:p>","DOI":"10.1002\/2211-5463.13699","type":"journal-article","created":{"date-parts":[[2023,8,22]],"date-time":"2023-08-22T15:59:26Z","timestamp":1692719966000},"page":"2020-2034","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Store\u2010operated calcium entry mediates hyperalgesic responses during neuropathy"],"prefix":"10.1002","volume":"13","author":[{"given":"Wei","family":"Wang","sequence":"first","affiliation":[{"name":"Shanghai Mental Health Center Shanghai Jiao Tong University School of Medicine  Shanghai China"},{"name":"Shanghai Key Laboratory of Psychotic Disorders  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