The peristaltic reflex is initiated by release of the sensory transmitter calcitonin gene-related peptide (CGRP) following distension of mechanical stimulation of the mucosa. Chemical stimulation of the mucosa by intraluminal nutrients also likely influences the peristaltic reflex although little is known of this process. A growing literature has demonstrated the presence of classical taste receptor components in enteroendocrine cells of the gut although it is unclear if they are involved. AIM: to determine if the classical umami receptor ligand, monosodium glutamate (MSG), induces peristalsis and to identify the mechanism. METHODS: Flat sheet preparations of rat colon were pinned in a 3-chambered organ bath in which ascending contraction and descending relaxation were measured in the orad and caudad compartments respectively. MSG alone and in the presence of inosine-5’ monophosphate (IMP) was added to the central sensory chamber; release of the CGRP was measured in this chamber by radioimmunoassay. Potentiation of the MSG response by IMP is well known to verify that a response is mediated by the T1R1/T1R3 umami taste receptor rather than an alternative amino acid-sensing receptor. RESULTS: Addition of MSG (10 mM) to the central compartment initiated the peristaltic reflex: ascending contraction orad and descending relaxation caudad. Concomitant with the initiation of peristalsis, MSG caused an increase (87±13 % increase above basal) in the release of CGRP from the mucosa in the central sensory compartment. The peristaltic response and the increase in CGRP release elicited by MSG were potentiated by the addition of IMP (1uM) indicative of activation of T1R1/T1R3 umami taste receptors, likely to be located on enteroendocrine cells. CONCLUSION: Luminal monosodium glutamate initiates a peristaltic reflex by interacting with T1R1/T1R3 receptors. Activation of these receptors leads ultimately to release of CGRP from enteric sensory neurons previously shown to mediate the colonic peristaltic reflex.
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© 2010 Published by Elsevier Inc.