Serotonin availability is increased in mucosa of guinea pigs with TNBS-induced colitis

David R. Linden, Jing Xian Chen, Michael D. Gershon, Keith A. Sharkey, Gary M. Mawe

Research output: Contribution to journalArticle

230 Scopus citations

Abstract

5-HT released from enterochromaffin cells acts on enteric nerves to initiate motor reflexes. 5-HT's actions are terminated by a serotonin reuptake transporter (SERT). In this study, we tested the hypothesis that inflammation leads to altered mucosal 5-HT signaling. Colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS), and experiments were conducted on day 6. 5-HT content, number of 5-HT-immunoreactive cells, and the proportion of epithelial cells that were 5-HT-immunoreactive increased twofold in colitis. The amount of 5-HT released under basal and stimulated conditions was significantly increased in colitis. SERT inhibition increased the 5-HT concentration in media bathing-stimulated control tissue to a level comparable to that of the stimulated colitis tissue. mRNA encoding SERT and SERT immunoreactivity were reduced during inflammation. Slower propulsion and reduced sensitivity to 5-HT-receptor antagonism were observed in colitis. These data suggest that colitis alters 5-HT signaling by increasing 5-HT availability while decreasing 5-HT reuptake. Altered 5-HT availability may contribute to the dysmotility of inflammatory bowel disease, possibly due to desensitization of 5-HT receptors.

Original languageEnglish (US)
Pages (from-to)G207-G216
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume285
Issue number1 48-1
DOIs
StatePublished - Jul 1 2003

Keywords

  • Enterochromaffin
  • Enteroendocrine
  • Inflammatory bowel disease
  • Motility
  • Serotonin transporter

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)

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