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

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

Research output: Contribution to journalArticle

98 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)565-574
Number of pages10
JournalNeurogastroenterology and Motility
Volume17
Issue number4
DOIs
StatePublished - Aug 2005
Externally publishedYes

Fingerprint

Serotonin Plasma Membrane Transport Proteins
Colitis
Serotonin
Enterochromaffin Cells
Inflammation
Sulfonic Acids
Intestinal Mucosa
Inflammatory Bowel Diseases
Mast Cells
Blood Vessels
Reflex
Mucous Membrane

Keywords

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

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology
  • Neuroscience(all)

Cite this

Serotonin transporter function and expression are reduced in mice with TNBS-induced colitis. / Linden, David R; Foley, K. F.; McQuoid, C.; Simpson, J.; Sharkey, K. A.; Mawe, Gary M.

In: Neurogastroenterology and Motility, Vol. 17, No. 4, 08.2005, p. 565-574.

Research output: Contribution to journalArticle

Linden, David R ; Foley, K. F. ; McQuoid, C. ; Simpson, J. ; Sharkey, K. A. ; Mawe, Gary M. / Serotonin transporter function and expression are reduced in mice with TNBS-induced colitis. In: Neurogastroenterology and Motility. 2005 ; Vol. 17, No. 4. pp. 565-574.
@article{4304014346b844aa986fbaea176bc278,
title = "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.",
keywords = "Enterochromaffin, Inflammatory bowel disease, Motility, Selective reuptake transporter, Serotonin transporter",
author = "Linden, {David R} and Foley, {K. F.} and C. McQuoid and J. Simpson and Sharkey, {K. A.} and Mawe, {Gary M.}",
year = "2005",
month = "8",
doi = "10.1111/j.1365-2982.2005.00673.x",
language = "English (US)",
volume = "17",
pages = "565--574",
journal = "Neurogastroenterology and Motility",
issn = "1350-1925",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Serotonin transporter function and expression are reduced in mice with TNBS-induced colitis

AU - Linden, David R

AU - Foley, K. F.

AU - McQuoid, C.

AU - Simpson, J.

AU - Sharkey, K. A.

AU - Mawe, Gary M.

PY - 2005/8

Y1 - 2005/8

N2 - 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.

AB - 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.

KW - Enterochromaffin

KW - Inflammatory bowel disease

KW - Motility

KW - Selective reuptake transporter

KW - Serotonin transporter

UR - http://www.scopus.com/inward/record.url?scp=23044439323&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=23044439323&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2982.2005.00673.x

DO - 10.1111/j.1365-2982.2005.00673.x

M3 - Article

C2 - 16078946

AN - SCOPUS:23044439323

VL - 17

SP - 565

EP - 574

JO - Neurogastroenterology and Motility

JF - Neurogastroenterology and Motility

SN - 1350-1925

IS - 4

ER -