| Project/Area Number |
21890304
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
TABUCHI Katsuhiko National Institute for Physiological Sciences, 大脳皮質機能研究系, 准教授 (20546767)
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| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥2,652,000 (Direct Cost: ¥2,040,000、Indirect Cost: ¥612,000)
Fiscal Year 2010: ¥1,261,000 (Direct Cost: ¥970,000、Indirect Cost: ¥291,000)
Fiscal Year 2009: ¥1,391,000 (Direct Cost: ¥1,070,000、Indirect Cost: ¥321,000)
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| Keywords | 自閉症 / シナプス / モデル動物 / Neuroligin / Neurexin / 電気生理学 / SDS-FRL法 / 疾患モデルマウス |
|---|
| Research Abstract |
To study the pathogenesis of autism, we analyzed the synaptic function in mouse models harboring Neuroligin-3 R451C mutation. We found that the synaptic transmission mediated by NMDA glutamate receptors was enhanced in the hippocampus of these mice and this was due to the increased number of the receptor on the synaptic membrane. In addition, we found morphological abnormalities in the mutant synapses. These findings may provide insight into understanding the pathopysiology and developing treatments of autism.
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