| Project/Area Number |
23500428
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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, ヘルスバイオサイエンス研究部, 特任教授 (50240916)
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| Co-Investigator(Kenkyū-buntansha) |
KAJI Ryuji 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (00214304)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ジストニア / 神経病理 / 機能解剖 / 線条体 / パーキンソニズム / ストリオゾーム / 臨床神経生理 / 脳内機能マッピング / 遺伝子改変モデル / フィリピン / 脳深部刺激 / 大脳基底核 / 定位脳手術 / DBS |
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| Research Abstract |
In the mammalian striatum, there exist two functional subdivisions termed as striosome and matrix compartments. We have proposed a hypothesis that an imbalanced activities between the striosome and matrix compartments may cause movement disorders that include dystonia. During the last 3 years, we found a selective loss of dopamine D1 receptor D1R and Golf expression in the striosomes in a transgenic mouse model with dystonia, and suggest that a loss of D1Rmediated signaling in the striosomes may cause dystonia symptoms. Moreover, our pathological study on the autopsied brains showed the defects in the neuropeptide NPY system in the striatum of the patients with DYT3 dystonia. Since NPY has a protective role against glutamate receptor-mediated neurotoxicity and promotes striatal neurogenesis, this finding suggests that defects in the NPY system may underlie the genesis of progressive striatal generation that primarily occurs in the striosome compartment.
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