| Project/Area Number |
21790106
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Institute for Developmental Research, Aichi Human Service Center |
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Principal Investigator |
ITO Hidenori 愛知県心身障害者コロニー発達障害研究所, 神経制御学部, 主任研究員 (40311443)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 統合失調症 / ニューロン / スパイン / dysbindin-1 / 細胞周期 / 神経細胞 / WAVE2 |
|---|
| Research Abstract |
We attempted to clarify physiological roles of dysbindin-1, a schizophrenia-related molecule, in nervous tissues. From immunofluorescence analysis, we found that dysbindin-1 localized at dendritic spines in primary cultured rat hippocampal neurons. RNAi-mediated dysbindin-1 knockdown led to the generation of abnormally elongated immature dendritic protrusions. We identified WAVE2 as a binding partner for dysbindin-1. We also found that Abi-1, a binding molecule for WAVE2 involved in spine development, interacts with dysbindin-1. While dysbindin-1, WAVE2 and Abi-1 formed ternary complex, dysbindin-1 promoted the WAVE2/Abi-1 complex formation. These results indicate possible roles of dysbindin-1 in the regulation of dendritic spine morphogenesis through the interaction with WAVE2 and Abi-1.
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