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Different Forms of AMPA Receptor Mediated LTP and Their Correlation to the Spatial Working Memory Formation

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Shimshek,  Derya R.
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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Schupp,  Bettina
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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Layer,  Liliana E.
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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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Shimshek, D. R., Bus, T., Schupp, B., Jensen, V., Marx, V., Layer, L. E., et al. (2017). Different Forms of AMPA Receptor Mediated LTP and Their Correlation to the Spatial Working Memory Formation. Frontiers in Molecular Neuroscience, 10: 214, pp. 1-11. doi:10.3389/fnmol.2017.00214.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002D-C931-4
Abstract
Spatial working memory (SWM) and the classical, tetanus-induced long-term potentiation (LTP) at hippocampal CA3/CA1 synapses are dependent on L-α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPARs) containing GluA1 subunits as demonstrated by knockout mice lacking GluA1. In GluA1 knockout mice LTP and SWM deficits could be partially recovered by transgenic re-installation of full-length GluA1 in principle forebrain neurons. Here we partially restored hippocampal LTP in GluA1-deficient mice by forebrain-specific depletion of the GluA2 gene, by the activation of a hypomorphic GluA2(Q) allele and by transgenic expression of PDZ-site truncated GFP-GluA1(TG). In none of these three mouse lines, the partial LTP recovery improved the SWM performance of GluA1-deficient mice suggesting a specific function of intact GluA1/2 receptors and the GluA1 intracellular carboxyl-terminus in SWM and its associated behavior.