{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T04:35:10Z","timestamp":1791261310555,"version":"4.1.0"},"reference-count":48,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2015,9,4]],"date-time":"2015-09-04T00:00:00Z","timestamp":1441324800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["G.0341.13"],"award-info":[{"award-number":["G.0341.13"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003130","name":"Fonds Wetenschappelijk Onderzoek","doi-asserted-by":"publisher","award":["G.0249.09N"],"award-info":[{"award-number":["G.0249.09N"]}],"id":[{"id":"10.13039\/501100003130","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Visceral hypersensitivity is a main characteristic of functional bowel disorders and is mediated by both peripheral and central factors. We investigated whether enhanced splanchnic afferent signaling <jats:italic>in\u00a0vitro<\/jats:italic> is associated with visceral hypersensitivity <jats:italic>in\u00a0vivo<\/jats:italic> in an acute and postinflammatory rat model of colitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Trinitrobenzene sulfonic acid (<jats:styled-content style=\"fixed-case\">TNBS<\/jats:styled-content>)\u2010colitis was monitored individually by colonoscopy to confirm colitis and follow convalescence and endoscopic healing in each rat. Experiments were performed in controls, rats with acute colitis and in postcolitis rats. Colonic afferent mechanosensitivity was assessed <jats:italic>in\u00a0vivo<\/jats:italic> by quantifying visceromotor responses (<jats:styled-content style=\"fixed-case\">VMR<\/jats:styled-content>s), and by making extracellular afferent recordings from splanchnic nerve bundles <jats:italic>in\u00a0vitro<\/jats:italic>. Multiunit afferent activity was classified into single units identified as low threshold (<jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>), wide dynamic range (<jats:styled-content style=\"fixed-case\">WDR<\/jats:styled-content>), high threshold (<jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>), and mechanically insensitive afferents (<jats:styled-content style=\"fixed-case\">MIA<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>During acute <jats:styled-content style=\"fixed-case\">TNBS<\/jats:styled-content>\u2010colitis, <jats:styled-content style=\"fixed-case\">VMR<\/jats:styled-content>s were significantly increased and splanchnic nerve recordings showed proportionally less <jats:styled-content style=\"fixed-case\">MIA<\/jats:styled-content> and increased <jats:styled-content style=\"fixed-case\">WDR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content> afferents. Acute colitis gave rise to an enhanced spontaneous activity of both <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MIA<\/jats:styled-content> and augmented afferent mechanosensitivity in <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> WDR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content> afferents. Postcolitis, <jats:styled-content style=\"fixed-case\">VMR<\/jats:styled-content>s remained significantly increased, whereas splanchnic nerve recordings showed that the proportion of <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> WDR<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> HT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MIA<\/jats:styled-content> had normalized to control values. However, <jats:styled-content style=\"fixed-case\">LT<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">MIA<\/jats:styled-content> continued to show increased spontaneous activity and <jats:styled-content style=\"fixed-case\">WDR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content> remained sensitized to colorectal distension.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>Visceral hypersensitivity <jats:italic>in\u00a0vivo<\/jats:italic> is associated with sensitized splanchnic afferent responses both during acute colitis and in the postinflammatory phase. However, splanchnic afferent subpopulations are affected differentially at both time points.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.12667","type":"journal-article","created":{"date-parts":[[2015,9,4]],"date-time":"2015-09-04T11:39:45Z","timestamp":1441366785000},"page":"1709-1720","source":"Crossref","is-referenced-by-count":12,"title":["Mechanisms contributing to visceral hypersensitivity: focus on splanchnic afferent nerve signaling"],"prefix":"10.1111","volume":"27","author":[{"given":"A.","family":"Deiteren","sequence":"first","affiliation":[{"name":"Laboratory of Experimental Medicine and Pediatrics Division of Gastroenterology University of Antwerp Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. G.","family":"De Man","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Medicine and Pediatrics Division of Gastroenterology University of Antwerp Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C.","family":"Keating","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences University of Sheffield Sheffield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W.","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences University of Sheffield Sheffield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H. U.","family":"De Schepper","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Medicine and Pediatrics Division of Gastroenterology University of Antwerp Antwerp Belgium"},{"name":"Department of Gastroenterology and Hepatology Antwerp University Hospital Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. A.","family":"Pelckmans","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Medicine and Pediatrics Division of Gastroenterology University of Antwerp Antwerp Belgium"},{"name":"Department of Gastroenterology and Hepatology Antwerp University Hospital Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. M.","family":"Francque","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Medicine and Pediatrics Division of Gastroenterology University of Antwerp Antwerp Belgium"},{"name":"Department of Gastroenterology and Hepatology Antwerp University Hospital Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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