| Project/Area Number |
21659018
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Kanazawa University |
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Principal Investigator |
YONEDA Yukio 金沢大学, 薬学系, 教授 (50094454)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,280,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2009: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | ミトコンドリア / 神経細胞死 / NMDA / グルタミン酸 / 脳虚血 / NMDAレセプター / UCP2 / 人口チャネル / Ca2+蛍光イメージング / NMDA受容体 / ミトコンドリア膜電位 / ミトコンドリア内カルシウム濃度 / mPTP / 海馬神経細胞 / 細胞内遊離カルシウム濃度 |
|---|
| Research Abstract |
Glutamate neurotoxicity was found to at least in part involve mitochondrial membrane potential disruption, mPTP orchestration, mitochondrial free Ca^<2+> levels and UCP2 expression in rat hippocampal and cortical neurons. In HEK293 cells with acquired NMDAR channels and overexpressed UCP2, a more marked increase was seen in mitochondrial free Ca^<2+> levels, in addition to more severe cell death, after the exposure to NMDA than in cells without UCP2 overexpression. Accordingly, UCP2 could play a role as a determinant of the neurotoxicity mediated by NMDAR through a mechanism related to the modulation of mitochondrial free Ca^<2+> levels in neurons.
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