| Project/Area Number |
24700413
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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 |
Fusional basic brain science
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| Research Institution | Kumamoto University |
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Principal Investigator |
TOMITA Jun 熊本大学, 生命科学研究部, 研究員 (40432231)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | ショウジョウバエ / 睡眠 / 覚醒 / カルシニューリン / NMDA型グルタミン酸受容体 / シナプス恒常性仮説 / 断眠 / ミトコンドリア |
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| Research Abstract |
We have previously reported that calcineurin (Ca2+/calmodulin-dependent protein phosphatase) regulates sleep in Drosophila. Pan-neuronal calcineurin knockdown significantly decreases sleep. However, we could not identify a specific brain region important for reducing sleep by calcineurin knockdown, suggesting that ubiquitous calcineurin activity in the brain is involved in sleep regulation. We found that the amount of rebound sleep was significantly increased in calcineurin RNAi flies compared to control flies. Thus, we hypothesize that calcineurin plays a role in the synaptic homeostasis hypothesis of sleep regulation. To understand calcineurin function in the synaptic homeostasis hypothesis, we examined the relationship between mitochondrial dynamics in neurons and sleep. Although pan-neuronal impairment of mitochondrial transport significantly increased sleep, mitochondrial distribution in circadian clock neurons was not affected by calcineurin knockout.
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