| Project/Area Number |
17002013
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| Research Category |
Grant-in-Aid for Specially Promoted Research
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Doshisha University (2007)
The University of Tokyo (2005-2006) |
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Principal Investigator |
TAKAHASHI Tomoyuki Doshisha University, Faculty of Life and Medical Sciences, Professor (40092415)
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| Co-Investigator(Kenkyū-buntansha) |
TUJIMOTO Tetsuhiro University of Tokyo, Graduate School of Medicine, Lecturer (40212055)
齋藤 直人 東京大学, 大学院医学系研究科, 講師 (90334226)
堀 哲也 東京大学, 大学院医学系研究科, 助手 (70396703)
小池 真紀 (谷 真紀) 北海道大学, 大学院・医学系研究科, 助手 (60396702)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥281,970,000 (Direct Cost: ¥216,900,000、Indirect Cost: ¥65,070,000)
Fiscal Year 2007: ¥89,830,000 (Direct Cost: ¥69,100,000、Indirect Cost: ¥20,730,000)
Fiscal Year 2006: ¥96,070,000 (Direct Cost: ¥73,900,000、Indirect Cost: ¥22,170,000)
Fiscal Year 2005: ¥96,070,000 (Direct Cost: ¥73,900,000、Indirect Cost: ¥22,170,000)
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| Keywords | Potassium channcl / Ca^<2+>channel inactivation / Calyx of Held / Postnatal development / Transmitter release / Calmodulin / AMPA receptors / Residual Ca^<2+> / Caチャネル不活性化 / Caチャネル / 神経終末端 / 5-HTレセプター / ステロイド / GTP結合タンパク質 / タキフィラキシー / シナプス小胞 / エンドサイトーシス / 伝達効率 / AMPA受容体 |
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| Research Abstract |
(1) During the postnatal development Kv3 and Kv1 currents underwent a parallel increase, and became faster. Specific block of these channels indicated that the developmental changes of Kv3 and Kv1 contribute to establishment of reliable firing at high frequency, and stabilizing the nerve terminal, respectively (Nakamura & Takahashi, 2007)
(2) Bath-applied 4-CmC markedly increased the EPSC amplitude at the calyx of Held by inhibiting presynaptic voltage-gated K+currents, with no effect on voltage-gated Ca2+currents (Suzuki et al, 2007).
(3) The CaM-dependent IpCa inactivation during low-frequency stimulation, and the ensuing synaptic depression, occurs only at immature calyces, when a high intra-terminal Ca2+concentration can be attained during low frequency stimulation (Nakamura et al, 2008).
(4) Contribution of AMPAR desensitization to paired-pulse depression decreased after hearing onset, concomitantly with a developmental declines of GluR1 expression and transmitter release probability, indicating that both pre- and postsynaptic mechanisms contribute to the involvement of AMPAR desensitization in short-term synaptic depression (Koike-Tani et al, 2008).
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