2011 Fiscal Year Final Research Report
Glutamate receptor dynamism in the brain functions and diseases
| Project/Area Number |
21300118
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NATSUME Rie 新潟大学, 脳研究所, 技術職員 (60467082)
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| Co-Investigator(Renkei-kenkyūsha) |
ABE Manabu 新潟大学, 脳研究所, 准教授 (10334674)
YAMAZAKI Maya 新潟大学, 脳研究所, 助教 (70401768)
WATANABE Masahiko 北海道大学, 大学院・医学研究科, 教授 (70210945)
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| Research Collaborator |
KANO Masanobu 東京大学, 大学院・医学系研究科, 教授 (40185963)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 分子 / 細胞神経科学 |
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| Research Abstract |
The objective of this study is to verify a working hypothesis that the expression and stability of glutamate receptors, including(further) transition to synapses and removal, are responsible for(are involved in) different modes of neuronal regulation depending on each kind of brain cells and regions, which transforms simple inputs into various types of outputs, thus underlying complex neuronal expressions. For this purpose, we established floxed mice of 4 AMPA-type-and 4 NMDA-type-glutamate receptors, as well as several kinds of synaptic functional molecules floxed mice. We also generated Cre-driver mice such as GAD67-Cre mouse. By inter-crossing these mice, we have clarified that a GluN2B subunit is crucial for synaptic functional expression of NMDA-type receptors in a CA3 area of hippocampus, and that TARPγ-2 andγ-7 are essential for the expression of AMPA type receptors in cerebellum. We have also shown that at developing synapses GluN2A and GluN2B suppress AMPA receptors in their own mode, by using a single-cell NMDA receptor subunit deleted mouse.
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