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Glutamatergic plasticity by synaptic delivery of GluR-Blong-containing AMPA receptors

MPS-Authors
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Kolleker,  Aleksandre
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Zhu,  J. Julius
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Schupp,  Bettina
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Mack,  Volker
Department of Molecular Neurobiology, 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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Köhr,  Georg
Department of Molecular Neurobiology, 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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Osten,  Pavel
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Kolleker, A., Zhu, J. J., Schupp, B., Qin, Y., Mack, V., Borchardt, T., et al. (2003). Glutamatergic plasticity by synaptic delivery of GluR-Blong-containing AMPA receptors. Neuron, 40(6), 1199-1212. doi:10.1016/S0896-6273(03)00722-0.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0029-BA5C-7
Abstract
Activity-driven delivery of AMPA receptors is proposed to mediate glutamatergic synaptic plasticity, both during development and learning. In hippocampal CA1 principal neurons, such trafficking is primarily mediated by the abundant GluR-A subunit. We now report a study of GluR-B(long), a C-terminal splice variant of the GluR-B subunit. GluR-B(long) synaptic delivery is regulated by two forms of activity. Spontaneous synaptic activity-driven GluR-B(long) transport maintains one-third of the steady-state AMPA receptor-mediated responses, while GluR-B(long) delivery following the induction of LTP is responsible for approximately 50% of the resulting potentiation at the hippocampal CA3 to CA1 synapses at the time of GluR-B(long) peak expression-the second postnatal week. Trafficking of GluR-B(long)-containing receptors thus mediates a GluR-A-independent form of glutamatergic synaptic plasticity in the juvenile hippocampus.