Investigation of Alteration of Active Zone Structure in the Neuronal Protective Function of Presynapse
Project/Area Number |
17H04983
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Single-year Grants |
Research Field |
Neurophysiology / General neuroscience
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Research Institution | Niigata University |
Principal Investigator |
Sugie Atsushi 新潟大学, 研究推進機構, 研究准教授 (50777000)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥24,310,000 (Direct Cost: ¥18,700,000、Indirect Cost: ¥5,610,000)
Fiscal Year 2019: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥14,950,000 (Direct Cost: ¥11,500,000、Indirect Cost: ¥3,450,000)
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Keywords | シナプス / ショウジョウバエ / 神経変性 / アクティブゾーン / WNT / 活性帯 |
Outline of Final Research Achievements |
To quantify a variety of synaptic changes, we established a semi-automated technique for quantifying synapses on the photoreceptor axons (J. Vis. Exp., 2017). By developing this method, we found that synaptic loss occurred before neurodegeneration and that the divergent canonical WNT pathway is involved in maintaining the neuronal circuit. Based on the results of a series of synapse studies, we have published a review that summarizes the phenomena and mechanisms by which synaptic structure is functionally changed by neural activity (Neural Dev., 2018). We also established a recording system for individual activity in Drosophila and described circadian rhythms during stress in a constant light environment that induced degeneration of the photoreceptor axons (Sci. Rep., 2019).
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Academic Significance and Societal Importance of the Research Achievements |
私たちが樹立したショウジョウバエ神経変性モデルを用いて、シナプスに異常が生じたときに、その神経回路の構造・機能を正常に戻す仕組みの一端を明らかにした。本研究課題の達成によって将来的には、神経変性疾患の超早期に活性化する細胞維持機構を標的にしたバイオマーカーの開発や、シナプス維持を誘導する薬剤スクリーニングのための本研究モデルの使用等、神経変性疾患への早期介入に期待できる。
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Report
(4 results)
Research Products
(6 results)