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Forebrain-specific glutamate receptor B deletion impairs spatial memory but not hippocampal field long-term potentiation

MPS-Authors
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Shimshek,  Derya R.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Celikel,  Tansu
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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Bus,  Thorsten
Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), 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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Marx,  Verena
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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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Shimshek, D. R., Jensen, V., Celikel, T., Geng, Y., Schupp, B., Bus, T., et al. (2006). Forebrain-specific glutamate receptor B deletion impairs spatial memory but not hippocampal field long-term potentiation. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 26(33), 8428-8440. doi:10.1523/JNEUROSCI.5410-05.2006.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002A-EDC4-0
Abstract
We demonstrate the fundamental importance of glutamate receptor B (GluR-B) containing AMPA receptors in hippocampal function by analyzing mice with conditional GluR-B deficiency in postnatal forebrain principal neurons (GluR-B(deltaFb)). These mice are as adults sufficiently robust to permit comparative cellular, physiological, and behavioral studies. GluR-B loss induced moderate long-term changes in the hippocampus of GluR-B(deltaFb) mice. Parvalbumin-expressing interneurons in the dentate gyrus and the pyramidal cells in CA3 were decreased in number, and neurogenesis in the subgranular zone was diminished. Excitatory synaptic CA3-to-CA1 transmission was reduced, although synaptic excitability, as quantified by the lowered threshold for population spike initiation, was increased compared with control mice. These changes did not alter CA3-to-CA1 long-term potentiation (LTP), which in magnitude was similar to LTP in control mice. The altered hippocampal circuitry, however, affected spatial learning in GluR-B(deltaFb) mice. The primary source for the observed changes is most likely the AMPA receptor-mediated Ca2+ signaling that appears after GluR-B depletion, because we observed similar alterations in GluR-B(QFb) mice in which the expression of Ca2+-permeable AMPA receptors in principal neurons was induced by postnatal activation of a Q/R-site editing-deficient GluR-B allele.