Investigation of synaptic maintenance mechanisms via inositol trisphosphate signaling in neurons and glial cells
| Project/Area Number |
23689015
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OKUBO Yohei 東京大学, 医学(系)研究科(研究院), 講師 (40422282)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥27,430,000 (Direct Cost: ¥21,100,000、Indirect Cost: ¥6,330,000)
Fiscal Year 2013: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
Fiscal Year 2012: ¥8,710,000 (Direct Cost: ¥6,700,000、Indirect Cost: ¥2,010,000)
Fiscal Year 2011: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
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| Keywords | 脳・神経 / イノシトール三リン酸 / カルシウム / mGluR / アストロサイト / シナプス |
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| Research Abstract |
Synaptic functions should be maintained for the stable information processing in the brain. It is recognized that the shut down of experience inputs result in the attenuation of corresponding brain functions. We thus set out to investigate mechanisms underlying the synaptic maintenance mediated by ongoing experience-dependent inputs.
Whisker deprivation in mature mice induced the attenuation of synaptic strength in the neocortex. We revealed that the shut down of metabotropic glutamate receptor and following inositol trisphosphate (IP3) signaling in neurons is involved in this deprivation-induced attenuation. Therefore, IP3 signaling induced by ongoing whisker inputs is indispensable for the maintenance of synaptic functions.
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Report
(4 results)
Research Products
(32 results)
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[Journal Article] Calcium-dependent N-cadherin up-regulation mediates reactive astrogliosis and neuroprotection after brain injury2013
Author(s)
Kanemaru, K., Kubota, J., Sekiya, H., Hirose, K., Okubo, Y. and Iino, M
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Journal Title
Proc Natl Acad Sci USA
Volume: 110
Issue: 28
Pages: 11612-11617
DOI
Related Report
Peer Reviewed
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