Mechanisms of heat hyper- and hypoalgesia by peripheral metabotropic glutamate receptors
Project/Area Number |
26460348
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Kanazawa Medical University |
Principal Investigator |
NISHIO Matomo 金沢医科大学, 医学部, 教授 (80156041)
|
Co-Investigator(Kenkyū-buntansha) |
益岡 尚由 金沢医科大学, 医学部, 講師 (80509307)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 代謝型グルタミン酸受容体 / 後根神経節 / 痛覚過敏 / TRPV1 / 後根神経節細胞 |
Outline of Final Research Achievements |
Wounds and inflammation cause glutamate release from primary sensory nerve afferents and damaged cells in the peripheral tissue. In this study, we have revealed that glutamate acts on metabotropic glutamate receptors 1 and 5 (mGluR1/5) in dorsal root ganglion neurons, resulting in potentiation of TRPV1 activities, inhibition of voltage-gated calcium channels and increase of neurons expressing functional TRPV1. These effects are closely associated to multiphasic modulation by glutamate of pain.
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Report
(4 results)
Research Products
(20 results)