2015 Fiscal Year Final Research Report
Analysis of the molecular and neuronal mechanisms for chronic itch in the central nervous system
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 |
Research Field |
Pain science
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Research Institution | Kansai Medical University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2016-03-31
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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 |
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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Free Research Field |
疼痛学
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