Serotonin transporter function and expression are reduced in mice with TNBS-induced colitis

D. R. Linden, K. F. Foley, C. McQuoid, J. Simpson, K. A. Sharkey, Gary M. Mawe

Research output: Contribution to journalArticlepeer-review

106 Scopus citations


Regulated release of serotonin (5-HT) from enterochromaffin (EC) cells activates neural reflexes that are involved in gut motility, secretion, vascular perfusion and sensation. The 5-HT-selective reuptake transporter (SERT) terminates serotonergic signalling in the intestinal mucosa. The aim of this investigation was to determine whether mucosal 5-HT content, release, and/or reuptake are altered in a murine model of immune cell-mediated colitis. Experiments were conducted 6 days after colitis was induced by 2,4,6-trinitrobenzene sulfonic acid, a time point when macroscopic and histological damage scores indicated significant inflammation. During inflammation, SERT transcript levels and immunoreactivity were reduced, and the uptake of [3H] 5-HT was impaired. Increases in mucosal 5-HT content and the number of 5-HT-immunoreactive mast cells in the lamina propria were also detected in the inflamed region, whereas EC cell numbers did not change. Mucosal 5-HT released under basal and stimulated conditions was unchanged in animals with colitis. These data suggest that murine colitis alters 5-HT signalling by increasing 5-HT availability through decreased 5-HT uptake by mucosal epithelial cells. These findings support the concept that altered 5-HT signalling could be a contributing factor in altered gut function and sensitivity in inflammatory bowel disease.

Original languageEnglish (US)
Pages (from-to)565-574
Number of pages10
JournalNeurogastroenterology and Motility
Issue number4
StatePublished - Aug 2005


  • Enterochromaffin
  • Inflammatory bowel disease
  • Motility
  • Selective reuptake transporter
  • Serotonin transporter

ASJC Scopus subject areas

  • Physiology
  • Endocrine and Autonomic Systems
  • Gastroenterology


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