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NEUROREGULATION AND MOTILITY
1Department of Anatomy and Neurobiology, University of Vermont College of Medicine, Burlington, Vermont 05405; 2Department of Anatomy and Cell Biology, Columbia University, New York, New York 10032; and 3Departments of Physiology and Biophysics and Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1
Submitted 12 November 2002 ; accepted in final form 19 December 2002
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.
inflammatory bowel disease; serotonin transporter; enterochromaffin; enteroendocrine; motility
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