| Project/Area Number |
26830024
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Institute of Physical and Chemical Research |
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Principal Investigator |
Matsui Asuka 国立研究開発法人理化学研究所, 脳科学総合研究センター, 研究員 (30599684)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 樹状突起 / バレル / 神経活性依存的 / 大脳皮質 / バレル皮質 / 子宮内電気穿孔法 / 初代神経細胞培養 |
|---|
| Outline of Final Research Achievements |
We previously reported that BTBD3 (BTB/POZ domain containing 3) is essential for dendrite patterning of spiny stellate neurons in mouse somatosensory barrel cortex. Dendrites with less input are removed by BTBD3, however, dendrites with higher input were resistant for BTBD3 dependent dendrite elimination. This suggests that BTBD3 determines dendrite specificity for removal/maintenance through sensing the difference of neuronal inputs. However, it remains unknown how BTBD3 senses neuronal inputs and controls dendrite morphology. This present study revealed that BTBD3 phosphorylation triggers Rho activation through BTBD3-plexin interaction. We also found that neuronal activity induces BTBD3 translocation to intermediate filaments, suggesting that BTBD3 binding to intermediate filaments stabilizes these high input dendrites even more. These results suggest that the different state of BTBD3 determines dendrite specificity for removal/maintenance.
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