2016 Fiscal Year Final Research Report
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(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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| 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 |
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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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| Free Research Field |
神経薬理学
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