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

Abstract  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.