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Recent advances in understanding the role of serotonin in gastrointestinal motility in functional bowel disorders: alterations in 5‐HT signalling and metabolism in human disease
Author(s) -
Spiller R.
Publication year - 2007
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.2007.00965.x
Subject(s) - enterochromaffin cell , irritable bowel syndrome , tegaserod , serotonin , nausea , enteric nervous system , medicine , carcinoid syndrome , gastroenterology , constipation , 5 ht receptor , vomiting , endocrinology , receptor
Serotonin (5‐hydroxytryptamine, 5‐HT) is present in abundance within the gut, most stored in enterochromaffin cell granules. It is released by a range of stimuli, most potently by mucosal stroking. Released 5‐HT stimulates local enteric nervous reflexes to initiate secretion and propulsive motility. It also acts on vagal afferents altering motility and in large amounts induces nausea. Rapid reuptake by a specific transporter (serotonin transporter, SERT) limits its diffusion and actions. Abnormally increased 5‐HT is found in a range of gastrointestinal disorders including chemotherapy‐induced nausea and vomiting, carcinoid syndrome, coeliac disease, inflammatory bowel disease and irritable bowel syndrome (IBS) with diarrhoea (IBS‐D), especially that developing following enteric infection. Impaired SERT has been described in IBS‐D and might account for some of the increase in mucosal 5‐HT availability. 5‐HT 3 receptor antagonists inhibit chemotherapy‐induced nausea and diarrhoea associated with both carcinoid syndrome and IBS. While IBS‐D is associated with increased 5‐HT postprandially, IBS with constipation (IBS‐C) is associated with impaired 5‐HT response and responds to 5‐HT 4 agonists such as Prucalopride and 5‐HT 4 partial agonists such as Tegaserod.