| Project/Area Number |
26430054
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
GOTO Satoshi 徳島大学, 大学院医歯薬学研究部(医学系), 特任教授 (50240916)
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| Co-Investigator(Kenkyū-buntansha) |
梶 龍兒 徳島大学, 大学院医歯薬学研究部(医学系), 教授 (00214304)
森垣 龍馬 徳島大学, 大学院医歯薬学研究部(医学系), 助教 (70710565)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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)
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| Keywords | 神経変性疾患 / ジストニア / 神経病理 / 線条体 / ストリオソーム / マトリックス / ドパミン / 機能解剖 / パーキンソニズム |
|---|
| Outline of Final Research Achievements |
In the mammalian striatum that plays a central role in the basal ganglia circuit, there exist two functional subdivisions known as striosome and matrix compartments. During the last 3 years, we found a selective loss of dopamine D1 receptor (D1R)-mediated signals in the striosome compartment in transgenic mouse and human disease models with dystonia. Moreover, we provided the evidence that striatal neurodegeneration causing dystonia might be associated with a lack of striosomal expression of neuroprotective molecules that include neuropeptide Y and postsynaptic density protein 95 (PSD-95). These findings corroborate with the hypothesis that deregulation of D1 signaling in the striosome compartment may underlie the genesis of dystonia.
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