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Serotonin transporter function and expression are reduced in mice with TNBS-induced colitis
D R Linden1, K F Foley, C McQuoid
1Department of Anatomy and Neurobiology, The University of Vermont College of Medicine, Burlington, VT 05405, USA.
Neurogastroenterology and Motility
|August 5, 2005
Summary
In colitis, the serotonin transporter (SERT) is reduced, impairing serotonin reuptake. This leads to increased serotonin availability, potentially altering gut function and sensitivity in inflammatory bowel disease.
Area of Science:
- Gastroenterology
- Neuroscience
- Immunology
Background:
- Serotonin (5-HT) released from enterochromaffin (EC) cells regulates gut functions via neural reflexes.
- The serotonin transporter (SERT) is crucial for terminating serotonergic signaling in the intestinal mucosa.
Purpose of the Study:
- To investigate alterations in mucosal serotonin content, release, and reuptake in a murine model of immune cell-mediated colitis.
Main Methods:
- Experiments were conducted 6 days post-induction of colitis using 2,4,6-trinitrobenzene sulfonic acid.
- Assessed SERT transcript levels, immunoreactivity, [3H] 5-HT uptake, mucosal 5-HT content, and mast cell counts.
Main Results:
- Colitis induced reduced SERT transcript levels and immunoreactivity, alongside impaired [3H] 5-HT uptake.
- Increased mucosal 5-HT content and 5-HT-immunoreactive mast cells were observed in inflamed regions.
- No significant changes in EC cell numbers or basal/stimulated mucosal 5-HT release were detected.
Conclusions:
- Murine colitis alters serotonin signaling by decreasing 5-HT reuptake, increasing its availability in the mucosa.
- Altered serotonin signaling may contribute to altered gut function and sensitivity in inflammatory bowel disease.