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DBI is highly expressed in SGCs of mice, rats, and humans, but not in sensory neurons or most other DRG-resident cells. Knockdown of DBI results in a robust mechanical hypersensitivity without major effects on other sensory modalities. In vivo overexpression of DBI in SGCs reduces sensitivity to mechanical stimulation and alleviates mechanical allodynia in neuropathic and inflammatory pain models. We further show that DBI acts as an unconventional agonist and positive allosteric modulator at the neuronal GABA\n                    <jats:sub>A<\/jats:sub>\n                    receptors, particularly strongly affecting those with a high-affinity benzodiazepine binding site. Such receptors are selectively expressed by a subpopulation of mechanosensitive DRG neurons, and these are also more enwrapped with DBI-expressing glia, as compared with other DRG neurons, suggesting a mechanism for a specific effect of DBI on mechanosensation. 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This communication modulates pain signaling and can be targeted therapeutically.\n                  <\/jats:p>","DOI":"10.1172\/jci176227","type":"journal-article","created":{"date-parts":[[2024,6,18]],"date-time":"2024-06-18T12:00:44Z","timestamp":1718712044000},"source":"Crossref","is-referenced-by-count":20,"title":["Peripheral gating of mechanosensation by glial diazepam binding inhibitor"],"prefix":"10.1172","volume":"134","author":[{"given":"Xinmeng","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pharmacology; The Key Laboratory of Neural and Vascular Biology, Ministry of Education; The Key Laboratory of New Drug Pharmacology and Toxicology, Hebei Medical University, Shijiazhuang, Hebei, China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arthur Silveira","family":"Prudente","sequence":"additional","affiliation":[{"name":"Pain Research Center, Department of Anesthesiology, University of Cincinnati Medical Center, Cincinnati, Ohio, 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