| Project/Area Number |
03404017
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Osaka University |
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Principal Investigator |
TSUMOTO Tadeharu Osaka University Medical School, Professor, 医学部, 教授 (50028619)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Hiromichi Osaka University Medical School, Lecturer, 医学部, 講師 (50154092)
畠 義郎 大阪大学, 医学部, 助手 (40212146)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥30,000,000 (Direct Cost: ¥30,000,000)
Fiscal Year 1993: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1992: ¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1991: ¥20,000,000 (Direct Cost: ¥20,000,000)
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| Keywords | Synaptic plasticity / Visual cortex / Long-term potentiation / Long-term depression / Development / Rat / Calcium / Memory |
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| Research Abstract |
In the developing visual cortex, repetitive stimulation of afferent pathways was reported to induce long-term potentiation (LTP) or long-term depression (LTD) of synaptic transmission in layr II/III of the cortex. It was not clearly known, however, what factors determine the direction of long-term changes in synaptic efficacy, i.e., LTP or LTD.The present results were designed to address this question.
Thin slices of the visual cortex were prepared from young rats (postnatal days 20-26) and loaded with a fluorescent Ca^<2+> indicator, rhod 2/AM.Changes in fluorescence intensity and field potentials evoked by test stimulation of layr IV were simultaneously recorded from layr II/III.
Tetanic stimulation consisting of 0.2 msec width pulses induced a massive increase in fluorescence intensity and LTP of field potentials, while weaker tetanus consisting of 0.1 msec pulses often induced a moderate rise of fluorescence and LTD of field potentials. There was a linear relationship between the magnitude of fluorescence rise and changes in peak amplitude of the field potentials. In sum, it is suggested that a rise of postsynaptic Ca^<2+> during synaptic inputs beyond a certain threshold induces LTP while a weak or moderate rise below the threshold induces LTD.
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