| Project/Area Number |
25460729
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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 | Kansai Medical University |
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Principal Investigator |
KATANO Tayo 関西医科大学, 医学部, 講師 (60469244)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Seiji 関西医科大学, 医学部, 教授 (80201325)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 神経障害性疼痛 / BEGAIN / プロテオミクス / 脊髄後角 / IIi層 / PSD / シナプス / 慢性疼痛 / 神経可塑性 |
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| Outline of Final Research Achievements |
Maintenance of neuropathic pain caused by peripheral nerve injury critically depends on the phosphorylation of GluN2B, a subunit of NMDA receptor, at Tyr1472 (Y1472). Here we took an advantage of comparative proteomic analysis between wild-type and knockin mice with a mutation of Y1472 to Phe of GluN2B (Y1472F-KI) to search for PSD proteins in the spinal dorsal horn that mediate signaling of neuropathic pain downstream of phosphorylated Y1472 GluN2B. We identified brain-enriched guanylate kinase-associated protein (BEGAIN) as increased protein in wild-type, but not in Y1472F-KI mouse after peripheral nerve injury by proteomic analysis.
BEGAIN was localized in spinal lamina IIi. Moreover, neuropathic pain, but not physiological pain was significantly attenuated in the knockout mice of BEGAIN. These results indicate that BEGAIN was involved in pathological pain transmission through NMDAR activation following the phosphorylation of GluN2B at Y1472 in spinal lamina IIi.
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