| Project/Area Number |
11680801
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
神経・脳内生理学
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| Research Institution | Tohoku University |
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Principal Investigator |
UMEMIVA Masashi Tohoku University, Neurophvsiology Research, associate, 大学院・医学系研究科, 助手 (50271911)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | NMDA / AMPA / Fluo-3 / Cortical neuron / Rat / Patch-clamp / EPSC / Calcium imaging / シナプス後電流 |
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| Research Abstract |
NMDA receptors (NMDAR) are highly calcium permeable and are negatively regulated by intracellular calcium during prolonged exposure to agonist. We have investigated whether calciummediated feedback occurs during single synaptic events mediated by transient exposure to glutamate. Examination of miniature EPSCs indicated that the decay kinetics of the NMDAR component was markedly slowed by the addition of exogenous calcium buffers (BAPTA and fluo-3). In contrast the AMPA receptor component of the miniature EPSC was unaffected by BAPTA.Slow on-rate calcium buffers, such as EGTA, did not alter the NMDAR component of the miniature EPSC.Addition of exogenous fast calcium buffers did not slow the deactivation kinetics of NR1/NR2A heteromers expressed in HEK-293 cells suggesting that the effect we observe may be specific to processes associated with synaptically activated receptors. Trial to trial amplitude variability of miniature calcium transients mediated by NMDARs increased with the injection of exogenous calcium buffers suggesting that the amplitude of calcium transients are maintained at a rather constant level by a calcium-mediated feedback mechanism.
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