| Project/Area Number |
09480241
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Osaka University |
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Principal Investigator |
TSUMOTO Tadaharu Osaka University graduate School of Medicine, Professor, 医学系研究科, 教授 (50028619)
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| Co-Investigator(Kenkyū-buntansha) |
HATA Yoshio Osaka University graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (40212146)
畠 義郎 大阪大学, 医学部, 助手 (20089882)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 1999: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1997: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | Brain / Neural circuits / Neurotrophin / Neuron / Synapse / Development / Long-term depression / Long-term potentiation |
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| Research Abstract |
In the developing visual cortex, neurotrophins such as brain-derived neurotrophic factor (BDNF) are suggested to play a role in activity-dependent plasticity of synaptic function. In particular, BDNF has been suggested to block a form of synaptic plasticity, long-term depression (LTD), in visual cortex. In this project we attempted to elucidate mechanisms underlying such a blocking action of BDNF using the whole-cell patch-clamp recording technique in visual cortical slices prepared from young rats. We found that 1) long-lasting, repetitive stimulation at 1 Hz for 10-15 min that was previously reported to induce LTD did not reliably induce LTD if postsynaptic neurons were voltage-clamped at the resting level, 2) to induced LTD, postsynaptic neurons should be depolarized in conjunction with low-frequency inputs, 3) exogenous BDNF at 20 ng/ml blocked LTD which is to be induced by such low-frequency, conjunctive stimulation, 4) endogenous BDNF served so as to prevent low-frequency inputs without postsynaptic depolarization from inducing LTD, and 5) such an action of BDNF was mediated by an activation of tyrosine kinases of TrkB receptors in presynaptic sites.
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