1991 Fiscal Year Final Research Report Summary
Mechanisms underlying control of developmental plasticity by glutamate receptros of NMDA type
| Project/Area Number |
01480125
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 Tadaharu Osaka University Medical School, Professor, 医学部, 教授 (50028619)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Hiromich Osaka University Medical School, Lecturer, 医学部, 講師 (50154092)
KUMURA Fumitaka Osaka University Medical School, Research Associate, 医学部, 助手 (00202044)
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| Project Period (FY) |
1989 – 1990
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| Keywords | NMDA receptor / Glutamate receptor / Synaptic plasticity / Visual cortex / Long-term potentiation / Long-term depression / Development / Rat |
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| Research Abstract |
Long-term potentiation (LTP) of synaptic efficacy is a well known example of a use-dependent synaptic plasticity in the mammalian brain. In the developing visual cortex In particular, LTP is proposed as a basis of environmental modifiability of visual cortical neurons during a "critical period" of postnatal development. Previous studies suggested that glutamate receptors of N-methyl-D-aspartate (NMDA) type may play a role in induction of LTP and an entry of Ca^<2+> into postsynaptic sites through NMDA receptor-linked channels may trigger processes for induction of LTP. However, there were no direct experimental data supporting this hypothesis in the developing visual cortex. In the present study, therefore, we attempted to test this hypothesis and found that the induction of LTP is blocked by the application of an NMDA receptor antagonist and further that an injection of a Ca^<2+>-chelator into visual cortical neurons leads to long-term depression (LTD) of their excitatory postsynaptic potentials (EPSPs) following tetanic afferent stimuli which in most of the slices tested, simultaneously induce LTP of field potentials derived from unchelated cells. These results suggest that the low concentration of postsynaptic, free Ca^<22+> associated which tetanic synaptic inputs may lead to LTD while a rise of Ca^<2+> through activated NMDA receptor-linked channels may lead to LTP.
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