| Project/Area Number |
26860389
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 痒み / NMDA受容体 / GRP / c-fos / NR2B / 大槽内投与 / 三叉神経 / 脊髄 / GluN2B / GRPR |
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| Outline of Final Research Achievements |
A variety of neurological disorders such as atopic dermatitis induce severe chronic itch, although it is currently not known what the underlying cellular and molecular mechanisms are. By using mice with a knock-in mutation of the Tyr1472 site of NR2B (Y1472F-KI mice), we demonstrated that phosphorylation of NR2B at Y1472 is important for trigeminal transmission of itch. In addition, intracisternal injection of various inhibitors and agonists revealed that NMDA receptor activation occurs upstream of the gastrin-releasing peptide (GRP)-GRP receptor pathway. Our finding open new avenues for the development of itch therapies and novel anti-itch drugs.
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