| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
We attempted to identify a novel neural circuit in the central complex regulating sleep-wake in Drosophila melanogaster and found a group of protocerebral bridge (PB) interneurons that promote sleep. Because the sleep-promoting PB interneurons had a physical connection with the already identified wake-promoting PB-FB-NO, the PB interneurons should inhibit the PB-FB-NO neurons.
We found that activation of T1 dopaminergic neurons projecting to PB using the temperature-sensitive dTrpA1 channel resulted in a significant reduction in sleep. Dopamine 2-like receptors (Dop2R) knockdown in the sleep-promoting PB interneurons significantly increased sleep, suggesting that T1 dopaminergic neurons promote wakefulness by inhibiting the sleep-promoting PB interneurons through D2 receptor signaling. In addition, we found that NMDA receptor-calcineurin signaling in the sleep-promoting PB interneurons is also involved in sleep regulation.
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