2003 Fiscal Year Final Research Report Summary
Study on Cross-talk of second messenger system in taste transduction
| Project/Area Number |
13660123
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
食品科学・栄養科学
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| Research Institution | Kyoto University |
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Principal Investigator |
HAYASHI Yukako Kyoto University, Graduate School of Agriculture, Assistant Professor, 農学研究科, 講師 (60212156)
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| Project Period (FY) |
2001 – 2003
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| Keywords | taste / umami / bitter / mouse / patch clamp / taste cells / palatability / taste nerve |
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| Research Abstract |
It has been suggested that second messenger system are involved in umami, bitter and sweet taste transduction.
Employing electrophysiological technique, I analyzed has bitter and umami transduction mechanism in mouse taste cells.
Umami taste has unique feature such as synergism between MSG and nucleotide. We have recorded the synergistic responses in the single taste cells to glutamate agonists-IMP mixture and reported that G protein is involved in umami transduction using the patch-clamp recording. Two putative G protein coupled receptors for glutamate have been identified, taste-mGluR4 and the amino acid receptor T1R1/T1R3 heterodimer. But, precise transduction mechanisms are still unknown. Using nerve recording, we measured response to MSG, IMP and a mixture of MSG and IMP in mouse circumvallate and foliate. The glossopharyngeal nerve responded to each amino acid and IMP slightly. When it was stimulated with the amino acid-IMP mixture solutions, the responses were was additive rather than the synergistic. The amino acid solution induced larger response in chords tympani nerve. Compared with the glossopharyngeal nerve, the response of MSG and L-AspNa increased notably in the chords tympani nerve. Furthermore, when IMP was added, L-AspNa shown the synergistic effect. These results suggest that T1R1/T1R3 received amino acid and contributed to the synergistic effect of umami taste.
Transduction of bitter taste of denatonium was suggested to involve cAMP and IP_3. Recording of effect of GDP-βs m inhibitor of phospholipase C or 8-Br-cAMP on denatonium response revealed that there is another pathway which is not related with G protein. Furthermore, the pathway is via release of intracellular Ca^<2+>. Bitterness from food is palatable for human, although bitter substances from toxins and medicines are unpalatable. We also suggested that there is different mechanisms between acceptable and non-acceptable bitterness using patch-clamp and two bottle preference test.
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