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However, the molecular mechanisms through which peripheral inflammation induces glycinergic disinhibition remain incompletely understood. Here we show that the protein tyrosine phosphatase-1B (PTP1B) is present at inhibitory synapses of spinal somatostatin-positive (SOM\n                    <jats:sup>+<\/jats:sup>\n                    ) interneurons, a key subpopulation of mechanosensory neurons that conveys nociceptive information. PTP1B directly binds to and dephosphorylates the glycine receptor \u03b11 subunit (GlyR \u03b11). Peripheral inflammation-induced hyperexpression of PTP1B competitively interrupts the interaction of GlyR \u03b11 with GPR39, leading to glycinergic disinhibition, enhanced excitatory output of SOM\n                    <jats:sup>+<\/jats:sup>\n                    interneurons, and behavioral hypersensitivity. Pharmacological activation of GPR39, however, could disrupt the PTP1B-GlyR \u03b11 interaction and resume GPR39 binding, resulting in reinstated glycinergic inhibition. Our findings uncover the important role of PTP1B in glycinergic disinhibition following peripheral inflammation and suggest a mechanistic model for dynamic regulation of glycinergic transmission by alternative interactions of GlyR \u03b11 with PTP1B and GPR39.\n                  <\/jats:p>","DOI":"10.1038\/s42003-026-10318-5","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T15:56:25Z","timestamp":1779292585000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Enhanced expression of spinal PTP1B contributes to peripheral inflammation- induced glycinergic disinhibition and mechanical pain"],"prefix":"10.1038","volume":"9","author":[{"given":"Hu-Hu","family":"Bai","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"Bai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao-Xue","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Bo","family":"Gao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xu","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia-Ning","family":"Dang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu-Xuan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi-Yang","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan-Ni","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiang-Ping","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7141-6597","authenticated-orcid":false,"given":"Zhan-Wei","family":"Suo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,20]]},"reference":[{"key":"10318_CR1","doi-asserted-by":"publisher","first-page":"899","DOI":"10.1515\/revneuro-2023-0037","volume":"34","author":"D Yao","year":"2023","unstructured":"Yao, D., Chen, Y. & Chen, G. 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