| Project/Area Number |
20700309
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neuroscience in general
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| Research Institution | National Institutes of Natural Sciences Okazaki Research Facilities |
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Principal Investigator |
SHIBASAKI Koji National Institutes of Natural Sciences Okazaki Research Facilities, 大学院・医学系研究科, 講師 (20399554)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2008: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | TRPV4 / 海馬 / 体温 / 脳内温度 / 神経興奮 / てんかん / 産学官 / 特許 / 温度センサー / リアルタイム測定 / 温度プローブ / 睡眠-覚醒 |
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| Research Abstract |
I found hippocampus strongly expressed TRPV4 in addition to choloid plexus, where TRPV4 expression was been reported. I considered that body temperature activates brain TRPV4, and the activation might contribute to depolarization of the resting membrane potential (RMP). I compared the RMP between wild-type and TRPV4-deficient neurons at 37℃, and found the wild-type RMP was approximately 5 mV more depolarized than the TRPV4-deficient RMP. I also performed current-injection experiments in both neurons, and found that TRPV4-deficient neurons required much bigger currents to get their firing. Furthermore, I found that glutamate-induced Ca^<2+> influx in wild-type neurons was much bigger than that in TRPV4-deficient neurons at 37℃. APV (a blocker of NMDA receptors) inhibited the enhancement of glutamate-induced Ca^<2+> influx in wild-type neurons at 37℃, suggesting that body temperature depolarized RMP near the thresholds for NMDA receptor activation compared with room temperature condition. Therefore, I conclude that TRPV4 is activated by body temperature in hippocampus, and produces proper environments for their firing.
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