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Hippocampal GluA1 expression in Gria1−/− mice only partially restores spatial memory performance deficits

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Freudenberg,  Florian
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Resnik,  Evgeny
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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

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Citation

Freudenberg, F., Resnik, E., Kolleker, A., Celikel, T., Sprengel, R., & Seeburg, P. H. (2016). Hippocampal GluA1 expression in Gria1−/− mice only partially restores spatial memory performance deficits. Neurobiology of learning and memory, 135, 83-90. doi:10.1016/j.nlm.2016.07.005.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002C-366C-7
Abstract
Spatial working memory (SWM) is an essential cognitive function important for survival in a competitive environment. In rodents SWM requires an intact hippocampus and SWM expression is impaired in mice lacking the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluA1 (Gria1−/− mice). Here we used viral gene transfer to show that re-expression of GluA1 in the hippocampus can affect the behavioral performance of GluA1 deficient mice. We found that Gria1−/− mice with hippocampus-specific rescue of GluA1 expression (Gria1Hpc mice) are more anxious, less hyperactive and only partly impaired in SWM expression in the Y-maze spatial novelty preference paradigm compared to Gria1−/− mice. However, Gria1Hpc mice still express SWM performance deficits when tested in the rewarded alternation T-maze task. Thus, the restoration of hippocampal function affects several behaviors of GluA1 deficient mice – including SWM expression – in different tasks. The virus-mediated GluA1 expression in Gria1−/− mice is not sufficient for a comprehensive SWM restoration, suggesting that both hippocampal as well as extra-hippocampal GluA1-containing AMPA receptors contribute to SWM.