Distinct effects of AMPAR subunit depletion on spatial memory.

Autor:	Eltokhi A; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany.; Department of Pharmacolog, University of Washington, Seattle, WA, USA., Bertocchi I; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany.; Department of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.; Neuroscience Institute - Cavalieri-Ottolenghi Foundation (NICO), Laboratory of Neuropsychopharmacology, Regione Gonzole 10, Orbassano, 10043 Torino, Italy., Rozov A; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany.; Institute of Neuroscience, Lobachevsky State University of Nizhniy, 603022 Novgorod, Russia.; Federal Center of Brain Research and Neurotechnology, 117997 Moscow, Russia., Jensen V; Department of Molecular Medicine, Division of Physiology, Institute of Basic Medical Sciences, University of Oslo, 0372 Oslo, Norway., Borchardt T; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany., Taylor A; Department of Experimental Psychology, University of Oxford, Oxford, UK., Proenca CC; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany., Rawlins JNP; Department of Experimental Psychology, University of Oxford, Oxford, UK., Bannerman DM; Department of Experimental Psychology, University of Oxford, Oxford, UK., Sprengel R; Departments of Molecular Neurobiology and Physiology, Max Planck Institute for Medical Research, Heidelberg, Germany.
Jazyk:	angličtina
Zdroj:	IScience [iScience] 2023 Oct 01; Vol. 26 (11), pp. 108116. Date of Electronic Publication: 2023 Oct 01 (Print Publication: 2023).
DOI:	10.1016/j.isci.2023.108116
Abstrakt:	Pharmacological studies established a role for AMPARs in the mammalian forebrain in spatial memory performance. Here we generated global GluA1/3 double knockout mice ( Gria1/3 -/- ) and conditional knockouts lacking GluA1 and GluA3 AMPAR subunits specifically from principal cells across the forebrain ( Gria1/3 ΔFb ). In both models, loss of GluA1 and GluA3 resulted in reduced hippocampal GluA2 and increased levels of the NMDAR subunit GluN2A. Electrically-evoked AMPAR-mediated EPSPs were greatly diminished, and there was an absence of tetanus-induced LTP. Gria1/3 -/- mice showed premature mortality. Gria1/3 ΔFb mice were viable, and their memory performance could be analyzed. In the Morris water maze (MWM), Gria1/3 ΔFb mice showed profound long-term memory deficits, in marked contrast to the normal MWM learning previously seen in single Gria1 -/- and Gria3 -/- knockout mice. Our results suggest a redundancy of function within the pool of available ionotropic glutamate receptors for long-term spatial memory performance. Competing Interests: The authors declare no competing interests. (© 2023 Max Planck Institute for Medical Research.)
Databáze:	MEDLINE
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