{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T22:48:24Z","timestamp":1790376504585,"version":"4.1.0"},"reference-count":48,"publisher":"American Society for Clinical Investigation","issue":"11","funder":[{"name":"MII Tedco","award":["NA"],"award-info":[{"award-number":["NA"]}]},{"name":"Ruth Kirschstein NIH predoctoral Fellowship","award":["F31NS084646"],"award-info":[{"award-number":["F31NS084646"]}]},{"name":"Department of Defense (DoD) National Defense Science and Engineering Graduate (NDSEG) Fellowship","award":["NA"],"award-info":[{"award-number":["NA"]}]},{"DOI":"10.13039\/100005317","name":"the Abell Foundation","doi-asserted-by":"crossref","award":["NA"],"award-info":[{"award-number":["NA"]}],"id":[{"id":"10.13039\/100005317","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Blaustein Pain Research grant","award":["NA"],"award-info":[{"award-number":["NA"]}]},{"name":"NIH","award":["NIH R35 NS097306"],"award-info":[{"award-number":["NIH R35 NS097306"]}]},{"name":"the Amos Food Body and Mind Center at Johns Hopkins University","award":["NA"],"award-info":[{"award-number":["NA"]}]},{"name":"National Health and Medical Research Council of Australia (NHMRC) R.D. Wright Biomedical Research Fellowship","award":["APP1126378"],"award-info":[{"award-number":["APP1126378"]}]},{"name":"NHMRC Australia Project Grants","award":["1083480,1139366,1140297"],"award-info":[{"award-number":["1083480,1139366,1140297"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,6,7]]},"abstract":"<jats:p>\n                    Functional bowel disorder patients can suffer from chronic abdominal pain, likely due to visceral hypersensitivity to mechanical stimuli. As there is only a limited understanding of the basis of chronic visceral hypersensitivity (CVH), drug-based management strategies are ill defined, vary considerably, and include NSAIDs, opioids, and even anticonvulsants. We previously reported that the 1.1 subtype of the voltage-gated sodium (Na\n                    <jats:sub>V<\/jats:sub>\n                    ; Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1) channel family regulates the excitability of sensory nerve fibers that transmit a mechanical pain message to the spinal cord. Herein, we investigated whether this channel subtype also underlies the abdominal pain that occurs with CVH. We demonstrate that Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1 is functionally upregulated under CVH conditions and that inhibiting channel function reduces mechanical pain in 3 mechanistically distinct mouse models of chronic pain. In particular, we use a small molecule to show that selective Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1 inhibition (a) decreases sodium currents in colon-innervating dorsal root ganglion neurons, (b) reduces colonic nociceptor mechanical responses, and (c) normalizes the enhanced visceromotor response to distension observed in 2 mouse models of irritable bowel syndrome. These results provide support for a relationship between Na\n                    <jats:sub>V<\/jats:sub>\n                    1.1 and chronic abdominal pain associated with functional bowel disorders.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.121000","type":"journal-article","created":{"date-parts":[[2018,6,6]],"date-time":"2018-06-06T11:01:10Z","timestamp":1528282870000},"source":"Crossref","is-referenced-by-count":43,"title":["NaV1.1 inhibition can reduce visceral hypersensitivity"],"prefix":"10.1172","volume":"3","author":[{"given":"Juan","family":"Salvatierra","sequence":"first","affiliation":[{"name":"Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel","family":"Castro","sequence":"additional","affiliation":[{"name":"Visceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, 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Medical Research Institute, Adelaide, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grigori Y.","family":"Rychkov","sequence":"additional","affiliation":[{"name":"Visceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Australia."},{"name":"Centre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australian Health and Medical Research Institute, Adelaide, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annemie","family":"Deiteren","sequence":"additional","affiliation":[{"name":"Visceral Pain Research Group, Human Physiology, Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Australia."},{"name":"Centre for Nutrition and Gastrointestinal Diseases, Discipline of Medicine, University of Adelaide, South Australian Health and Medical Research Institute, Adelaide, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4059-2453","authenticated-orcid":true,"given":"Rana","family":"Rais","sequence":"additional","affiliation":[{"name":"Johns Hopkins Drug Discovery and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glenn F.","family":"King","sequence":"additional","affiliation":[{"name":"Institute for Molecular Bioscience, the University of Queensland, Brisbane, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara S.","family":"Slusher","sequence":"additional","affiliation":[{"name":"Johns Hopkins Drug Discovery and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, 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