| Project/Area Number |
17500248
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
NAKAMURA Tsutomu The University of Tokyo, Institute of Molecular and Cellular Biosciences, Research Associate, 分子細胞生物学研究所, 助手 (30302798)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | synapse / PSD / NMDA receptor / PSD-95 / SPAL-1 / learning / memory / spine / シグナル伝達 / 神経科学 / 脳・神経 |
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| Research Abstract |
In this study, we examined physiological roles of SPAL-1, a novel GAP for Rap-1/2, using SPAL-1-deficient mice. In particular, we focused on the significance of NMDA receptor/PSD-95/SPAL-1 interaction in synaptic plasticity.
1. SPAL-1-deficient mice showed impaired spatial learning in Morris water maze test and decreased cued fear response in fear conditioning test. This finding suggests that SPAL-1 is involved in hippocampus- or amygdale-dependent memory formation.
2. We found that conditioned eyeblink response is impaired in mice lacking SPAL-1, suggesting that functional link between SPAL-1 and NMDA receptors.
3. Electrophysiological analysis using hippocampal slices revealed enhanced LTP in hippocampal CA1 region in SPAL-1-deficient mice.
4. Electron microscopic analysis of brain sections revealed smaller spines and shorter PSD in mice lacking SPAL-1.
5. We further investigated the behavioral characteristics of SPAL-1-deficient mice and found increased locomotor activity in the open-field test.
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