{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:16:45Z","timestamp":1787015805534,"version":"build-2736575974"},"reference-count":33,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,4,17]],"date-time":"2013-04-17T00:00:00Z","timestamp":1366156800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      3 antagonists, such as ondansetron (Zofran), retard colonic transit and provide effective relief of symptoms of chronic diarrhea and diarrhea\u2010predominant irritable bowel syndrome (\n                      <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content>\n                      ), but the mechanism by which ondansetron retards transit is unclear. What is clear is that the frequency of colonic migrating motor complexes (\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      s) is reduced by ondansetron, which could account for reduced transit. Our aim was to determine whether an acute depletion of 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      from enteric neurons would inhibit spontaneous\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      s; and determine whether the sensitivity of ondansetron to reduce\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      frequency would change in a 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      \u2010depleted preparation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Mice were injected with reserpine, 24\u00a0h prior to euthanasia to deplete neuronally synthesized 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      . Mechanical recordings were made from proximal and mid\u2010distal regions of isolated whole mouse colon. Immunohistochemical staining for 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      was used to detect neuronal 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Reserpine depleted all detectable 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      from enteric nerves. In whole colons, with mucosa and submucosal plexus removed, the frequency and amplitude of spontaneous\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      s was not different between groups treated with or without reserpine. Surprisingly, in mucosa and submucosal plexus\u2010free preparations, ondansetron was equally or significantly more effective at inhibiting\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      frequency compared with control preparations (containing 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      ). Reserpine pretreatment had no effect on the sensitivity of ondansetron to inhibit\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      s.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions &amp; Inferences<\/jats:title>\n                    <jats:p>\n                      Endogenous 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      in enteric neurons (or the mucosa) is not required for the spontaneous generation or propagation of\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      s. Furthermore, the primary mechanism by which ondansetron inhibits\n                      <jats:styled-content style=\"fixed-case\">CMMC<\/jats:styled-content>\n                      frequency is not mediated via the mucosa, submucosal plexus or 5\u2010\n                      <jats:styled-content style=\"fixed-case\">HT<\/jats:styled-content>\n                      in myenteric neurons.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nmo.12136","type":"journal-article","created":{"date-parts":[[2013,4,17]],"date-time":"2013-04-17T22:07:18Z","timestamp":1366236438000},"page":"677-685","source":"Crossref","is-referenced-by-count":32,"title":["By what mechanism does ondansetron inhibit colonic migrating motor complexes: does it require endogenous serotonin in the gut wall?"],"prefix":"10.1111","volume":"25","author":[{"given":"N. J.","family":"Spencer","sequence":"first","affiliation":[{"name":"Discipline of Human Physiology Flinders Medical Center South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. J.","family":"Nicholas","sequence":"additional","affiliation":[{"name":"Discipline of Human Physiology Flinders Medical Center South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. C.","family":"Sia","sequence":"additional","affiliation":[{"name":"Discipline of Human Physiology Flinders Medical Center South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"Staikopoulos","sequence":"additional","affiliation":[{"name":"Department of Physiology University of Adelaide South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Kyloh","sequence":"additional","affiliation":[{"name":"Discipline of Human Physiology Flinders Medical Center South Australia Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. 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