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A juvenile form of postsynaptic hippocampal long-term potentiation in mice deficient for the AMPA receptor subunit GluR-A

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Kaiser,  Katharina
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Borchardt,  Thilo
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Rozov,  Andrej
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Burnashev,  Nail
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sakmann,  Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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引用

Jensen, V., Kaiser, K., Borchardt, T., Adelmann, G., Rozov, A., Burnashev, N., Brix, C., Frotscher, M., Andersen, P., Hvalby, Ø., Sakmann, B., Seeburg, P. H., & Sprengel, R. (2003). A juvenile form of postsynaptic hippocampal long-term potentiation in mice deficient for the AMPA receptor subunit GluR-A. The Journal of Physiology - London, 553(3), 843-856. doi:10.1113/jphysiol.2003.053637.


引用: https://hdl.handle.net/11858/00-001M-0000-0029-B992-4
要旨
In adult mice, long-term potentiation (LTP) of synaptic transmission at CA3-to-CA1 synapses induced by tetanic stimulation requires L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors containing GluR-A subunits. Here, we report a GluR-A-independent form of LTP, which is comparable in size to LTP in wild-type mice at postnatal day 14 (P14) but diminishes between P14 and P42 in brain slices of GluR-A-deficient mice. The GluR-A-independent form of LTP is sensitive to D(-)-2-amino-5-phosphonopentanoic acid (D-AP5), but lacks short-term potentiation (STP) and can also be observed in the pairing induction protocol. As judged by unaltered paired-pulse facilitation, this LTP form is postsynaptically expressed despite depleted extrasynaptic AMPA receptor pools with reduced levels of GluR-B, which accumulates in somata and synapses of CA1 pyramidal neurons in GluR-A-deficient mice. Our results show that in the developing hippocampus synaptic plasticity can be expressed by AMPA receptors lacking the GluR-A subunit.