| Project/Area Number |
20300119
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KIKKAWA Satoshi 神戸大学, 大学院・医学研究科, 講師 (90244681)
KATSUYAMA Yu 神戸大学, 大学院・医学研究科, 助教 (10359862)
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| Project Period (FY) |
2008 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥19,110,000 (Direct Cost: ¥14,700,000、Indirect Cost: ¥4,410,000)
Fiscal Year 2011: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2010: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2008: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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| Keywords | リーリン / Dab1 / reeler / yotari / 大脳皮質 / 層形成 / Dabl / リーラー / 層構成 / 層特異的マーカ / reelin / cerebral cortex / 層構築 / ヨタリ |
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| Research Abstract |
Previous studies have elucidated many genes that are expressed in specific layers of cortical layers. Among these genes we chose four genes, i. e., mSorLA, ROR-beta, ER81 and Tbr1 and studied phenotypes of cerebral neocortex of the reeler mouse. It has been long considered that the reeler cortex is cytoarchitectually reversed. We have demonstrated that compaction of neuronal components expressing each layer marker is affected in the reeler cortex, which resulted in intermingling of different cortical neurons and blurred cortical layers. The similar abnormalities were also recognized in the dorsal horn of the spinal cord, dorsal cochlear nucleus and cerebellar neocortex of the reeler mouse, suggesting Reelin is essential for compaction of neurons. In the reeler cortex, ROR-beta expressing neurons are not widely scattered, suggesting compaction of ROR-beta expressing neurons-is regulated by molecules other than Reelin protein. In the reeler olfactory bulb, the cytoarchitectural abnormality is also subtle, and therefore formation of this laminar structure is regulated by Reelin-independent molecules. In conclusion, we could not identified reversed laminar structures of the reeler cortex as repeatedly reported by many previous reports, and the reeler malformation is caused by the intriguing outcomes of several mechanisms relating to Reelin protein.
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