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1 Department of Anatomy and Neurobiology, The University of Vermont College of Medicine, Burlington, VT, USA
2 Department of Anatomy and Cell Biology, Columbia University, New York, NY, USA
3 Departments of Physiology and Biophysics, University of Calgary, Calgary, AB, Canada
* To whom correspondence should be addressed. E-mail: gary.mawe{at}uvm.edu.
5-HT, released from enterochromaffin (EC) cells, acts on enteric nerves to initiate motor reflexes. 5-HT's actions are terminated by a 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 at day six. 5-HT content, numbers of 5-HT-immunoreactive cells, and the proportion of epithelial cells that were 5-HT-immunoreactive increased two-fold 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.
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