BACKGROUND: l-amino acids, such as monosodium glutamate (MSG), activate the umami receptor T1R1/T1R3. We previously showed increased peristalsis in response to activation of T1R1/T1R3 by MSG in mouse colon. However, the expression and function of these receptors in the different regions of the stomach are not clear. METHODS: Mouse gastric smooth muscle cells (SMCs) were isolated and cultured in Dulbecco's Modified Eagle Medium. Expression of T1R1 and T1R3 was measured by RT-PCR and Western blot. The effect of MSG with and without inosine monophosphate (IMP, an allosteric activator of T1R1/T1R3) on acetylcholine (ACh)-induced contraction was measured in muscle strips and isolated SMCs by scanning micrometry. The effect of MSG with or without IMP on activation of G proteins and ACh-induced Ca2+ release was measured in SMCs. KEY RESULTS: Monosodium glutamate inhibited ACh-induced contractions in muscle strips from both antrum and fundus and the effect of MSG was augmented by IMP; the effects were concentration-dependent and not affected by the nitric oxide synthase inhibitor, L-NNA, or tetrodotoxin suggesting a direct effect on SMCs. In isolated gastric SMCs, T1R1 and T1R3 transcripts and protein were identified. Addition of MSG with or without IMP inhibited ACh-induced Ca2+ release and muscle contraction; the effect on contraction was blocked by pertussis toxin suggesting activation of Gαi proteins. MSG in the presence of IMP selectively activated Gαi2 . CONCLUSIONS AND INFERENCES: Umami receptors (T1R1/T1R3) are present on SMCs of the stomach, and activation of these receptors induces muscle relaxation by decreasing [Ca2+ ]i via Gαi2 .
BACKGROUND:l-amino acids, such as monosodium glutamate (MSG), activate the umami receptor T1R1/T1R3. We previously showed increased peristalsis in response to activation of T1R1/T1R3 by MSG in mouse colon. However, the expression and function of these receptors in the different regions of the stomach are not clear. METHODS:Mouse gastric smooth muscle cells (SMCs) were isolated and cultured in Dulbecco's Modified Eagle Medium. Expression of T1R1 and T1R3 was measured by RT-PCR and Western blot. The effect of MSG with and without inosine monophosphate (IMP, an allosteric activator of T1R1/T1R3) on acetylcholine (ACh)-induced contraction was measured in muscle strips and isolated SMCs by scanning micrometry. The effect of MSG with or without IMP on activation of G proteins and ACh-induced Ca2+ release was measured in SMCs. KEY RESULTS:Monosodium glutamate inhibited ACh-induced contractions in muscle strips from both antrum and fundus and the effect of MSG was augmented by IMP; the effects were concentration-dependent and not affected by the nitric oxide synthase inhibitor, L-NNA, or tetrodotoxin suggesting a direct effect on SMCs. In isolated gastric SMCs, T1R1 and T1R3 transcripts and protein were identified. Addition of MSG with or without IMP inhibited ACh-induced Ca2+ release and muscle contraction; the effect on contraction was blocked by pertussis toxin suggesting activation of Gαi proteins. MSG in the presence of IMP selectively activated Gαi2 . CONCLUSIONS AND INFERENCES: Umami receptors (T1R1/T1R3) are present on SMCs of the stomach, and activation of these receptors induces muscle relaxation by decreasing [Ca2+ ]i via Gαi2 .
Authors: Yu Wang; Vera Prpic; Gary M Green; Joseph R Reeve; Rodger A Liddle Journal: Am J Physiol Gastrointest Liver Physiol Date: 2002-01 Impact factor: 4.052
Authors: Hong Xu; Lena Staszewski; Huixian Tang; Elliot Adler; Mark Zoller; Xiaodong Li Journal: Proc Natl Acad Sci U S A Date: 2004-09-07 Impact factor: 11.205
Authors: Cheng-Hai Zhang; Lawrence M Lifshitz; Karl F Uy; Mitsuo Ikebe; Kevin E Fogarty; Ronghua ZhuGe Journal: PLoS Biol Date: 2013-03-05 Impact factor: 8.029