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Am J Clin Nutr 90: 747S-752S, 2009. First published July 1, 2009; doi:10.3945/ajcn.2009.27462J
American Journal of Clinical Nutrition, doi:10.3945/ajcn.2009.27462J
Vol. 90, No. 3, 747S-752S, September 2009

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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

Multiple receptors underlie glutamate taste responses in mice1,2,3,4

Keiko Yasumatsu, Nao Horio, Yoshihiro Murata, Shinya Shirosaki, Tadahiro Ohkuri, Ryusuke Yoshida and Yuzo Ninomiya

1 From the Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan.

2 Presented at the "100th Anniversary Symposium of Umami Discovery: The Roles of Glutamate in Taste, Gastrointestinal Function, Metabolism, and Physiology," held in Tokyo, Japan, September 10–13, 2008.

3 Supported by Grants-in-Aid 18077004 and 18109013 (to YN) from the Japan Society for the Promotion of Science.

4 Address correspondence and requests for reprints to Y Ninomiya, Section of Oral Neuroscience, Graduate School of Dental Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. E-mail: yuninom{at}dent.kyushu-u.ac.jp.

L-Glutamate is known to elicit a unique taste, umami, that is distinct from the tastes of sweet, salty, sour, and bitter. Recent molecular studies have identified several candidate receptors for umami in taste cells, such as the heterodimer T1R1/T1R3 and brain-expressed and taste-expressed type 1 and 4 metabotropic glutamate receptors (brain-mGluR1, brain-mGluR4, taste-mGluR1, and taste-mGluR4). However, the relative contributions of these receptors to umami taste reception remain to be elucidated. We critically discuss data from recent studies in which mouse taste cell, nerve fiber, and behavioral responses to umami stimuli were measured to evaluate whether receptors other than T1R1/T1R3 are involved in umami responses. We particularly emphasized studies of umami responses in T1R3 knockout (KO) mice and studies of potential effects of mGluR antagonists on taste responses. The results of these studies indicate the existence of substantial residual responses to umami compounds in the T1R3-KO model and a significant reduction of umami responsiveness after administration of mGluR antagonists. These findings thus provide evidence of the involvement of mGluRs in addition to T1R1/T1R3 in umami detection in mice and suggest that umami responses, at least in mice, may be mediated by multiple receptors.




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