Regulation of pain through inter-GPCR interplay
| Project/Area Number |
26460707
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
長谷川 麻衣子 鹿児島大学, 医歯学域医学系, 准教授 (20516637)
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| Co-Investigator(Renkei-kenkyūsha) |
INADA Eiichi 順天堂大学, 医学部, 教授 (40193552)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 疼痛 / シナプス / GPCR / 代謝型グルタミン酸受容体 / アデノシン受容体 / 神経細胞 / Gタンパク質共役型受容体 / 痛み / 感覚伝達 / 脊髄 / FRET |
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| Outline of Final Research Achievements |
Many reports suggest that multiple G protein-coupled receptor (GPCR)s form heteromeric complexes and cooperatively trigger atypical signaling that cannot be initiated by individual GPCRs on their own. Indeed, previous studies suggest that Adenosine A1 receptor (A1R) activation also modulates cellular responses that depend on type-1 metabotropic glutamate receptor (mGluR1). mGluR1 are involved in pain transmission and synaptic plasticity including cerebellar long-term depression (LTD). In this project, we indicated that mGluR1-A1R form heteromeric complex and these receptors mutually modulate each other by direct interaction. These findings indicate a new mechanism of cooperation between neuronal GPCRs to elicit atypical and intriguing cellular responses.
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Report
(4 results)
Research Products
(18 results)
