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

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.

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

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 Urheber:
Kolleker, Aleksandre1, Autor           
Zhu, J. Julius2, Autor           
Schupp, Bettina1, Autor           
Qin, Yi, Autor
Mack, Volker1, Autor           
Borchardt, Thilo1, Autor           
Köhr, Georg1, Autor           
Malinow, Roberto, Autor
Seeburg, Peter H.1, Autor           
Osten, Pavel1, Autor           
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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 Zusammenfassung: 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.

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Sprache(n): eng - English
 Datum: 2002-10-242003-10-232003-12-18
 Publikationsstatus: Erschienen
 Seiten: 14
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Titel: Neuron
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Cambridge, Mass. : Cell Press
Seiten: - Band / Heft: 40 (6) Artikelnummer: - Start- / Endseite: 1199 - 1212 Identifikator: ISSN: 0896-6273
CoNE: https://pure.mpg.de/cone/journals/resource/954925560565