| Project/Area Number |
15300105
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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 |
Neuroscience in general
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| Research Institution | Nagoya University |
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Principal Investigator |
KOMATSU Yukio Nagoya University, Research Institute of Environmental Medicine, Professor, 環境医学研究所, 教授 (90135343)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Yumiko Nagoya University, Research Institute of Environmental Medicine, Assistant Professor, 環境医学研究所, 助手 (10291907)
TAKADA Naoki Nagoya University, Research Institute of Environmental Medicine, Assistant Professor, 環境医学研究所, 助手 (60335007)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥16,100,000 (Direct Cost: ¥16,100,000)
Fiscal Year 2004: ¥5,100,000 (Direct Cost: ¥5,100,000)
Fiscal Year 2003: ¥11,000,000 (Direct Cost: ¥11,000,000)
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| Keywords | ihibitory cell / NMDA receptor / long-term potentiation / long-term-depression / excitatory synapse / synaptic plasticity / visual cortex / development |
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| Research Abstract |
It is considered that long-term synaptic modifications underlie experience-dependent maturation of visual cortical functions. Although long-term potentiation(LTP) and long-term depression(LTD) have been intensively studied in pyramidal cells sending excitatory outputs, almost no study has been conducted in inhibitory non-pyramidal cells. In this study, we investigated NMDA receptor-dependent long-term modifications in layer 2/3 inhibitory cells of developing rat visual cortical slices. Excitatory postsynaptic currents were recorded from visualized layer 2/3 non-pyramidal cells under a pharmacological blockade of inhibitory synaptic transmission using patch electrodes containing neurobiotin, which was used for later histological identification of inhibitory cells. High-frequency stimulation of presynaptic fibers failed to produce LTP as in case of pyramidal cells. We previously demonstrated that low-frequency (1 Hz) stimulation paired with postsynaptic depolarization (0 mV) for 100 sec produced LTP frequently in pyramidal cells. This paring stimulation failed to produce either LTP or LTD in inhibitory cells. However, when this pairing stimulation was continued for 15 minutes, LTP occurred in about one-fourth of cells and LTD occurred in almost the same number of cells. The remaining about half of cells underwent no changes. In fast spiking inhibitory cells, LTD occurred in about 2/3 of them although LTP never occurred. On the other hand, LTP occurred more frequently than LTD in regular spiking inhibitory cells. Therefore, NMDA receptor-dependent synaptic plasticity occurs also in inhibitory cells, although longer conditioning stimulation was required for inhibitory than excitatory cells. In addition, LTD as well as LTP occurred depending on subtypes of inhibitory cells, which is different from excitatory cells in which only LTP occurred.
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