1998 Fiscal Year Final Research Report Summary
Molecular mechanisms of synaptic plasticity at visual cortical inhibitory synapses
| Project/Area Number |
08458271
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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 | 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) |
EDAGAWA Yoshikuni Nagoya University, Research Institute of Environmental Medicine, Research Associ, 環境医学研究所, 助手 (50303607)
IWAMOTO Yumiko Nagoya University, Research Institute of Environmental Medicine, Research Associ, 環境医学研究所, 助手 (10291907)
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| Project Period (FY) |
1996 – 1998
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| Keywords | Synaptic plasticity / long-term potentiation / long-term depression / inhibitory synapse / visual cortex / GABA / development |
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| Research Abstract |
We studied molecular mechanisms underling long-term potentiation (LTP) and long-term depression (LTD) at inhibitory synapses in developing rat visual cortex, and obtained following results.
1. Inhibition of postsynaptic phospholipase C, IP_3 receptors or Ca^<2+> increase prevented the generation of LTP as did the blockade of GABA_B receptors. In addition, blockade of alphal adrenoceptors or 5-HT_2 receptors, which are coupled with IP_3 formation, reduced incidence of LTP.These results suggest that LTP induction requires the activation of postsynaptic GABA_B receptors and that its effect is mediated at least partly by facilitation of the monoamine-induced IP_3 formation, which then causes Ca^<2+> release from the internal stores in postsynaptic cells.
2. LTD was produced by repetitive firing of cells elicited by a postsynaptic injection of depolarizing current pulses. Induction of LTD was blocked by bath application of the L-type Ca^<2+> channel inhibitor nifedipine or by postsynaptic loading of a Ca^<2+> chelator BAPTA.In addition, LTD was produced by flash photolysis of caged Ca^<2+> in postsynaptic cells. These results suggest that postsynaptic Ca^<2+> increases due to the activation of L-type Ca^<2+> channels are sufficient to generate LTD.
3. LTP never occurred when slices were perfused with a control solution containing 2.4 mM Ca^<2+>, 1.3 mM Mg^<2+> and 6.2 mMK^+. LTP was consistently produced when [Ca^<2+>]。 was increased to 4 mM The incidence of LTP was also increased by reducing [K^+]。 which produces membrane hyperpolarization. In addition, LTP occurred in most of tested cells when charybdotoxin or Cs^+ which are known to block K^+ channels, was added to the control solution. Thus, it is likely that voltage-dependent K^+ channels, which are gated near resting membrane potentials and modulate Ca^<2+> entry, regulate the generation of LTP.
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Research Products
(10 results)
