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Different forms of AMPA receptor mediated LTP and their correlation to the spatial working memory formation

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 knock...

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Hauptverfasser: Shimshek, Derya R. (VerfasserIn) , Koehr, Georg (VerfasserIn) , Sprengel, Rolf (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 04 July 2017
In: Frontiers in molecular neuroscience
Year: 2017, Jahrgang: 10
ISSN:1662-5099
DOI:10.3389/fnmol.2017.00214
Online-Zugang:Verlag, kostenfrei, Volltext: http://dx.doi.org/10.3389/fnmol.2017.00214
Verlag, kostenfrei, Volltext: https://www.frontiersin.org/articles/10.3389/fnmol.2017.00214/full
Volltext
Verfasserangaben:Derya R. Shimshek, Thorsten Bus, Bettina Schupp, Vidar Jensen, Verena Marx, Liliana E. Layer, Georg Köhr and Rolf Sprengel
Beschreibung
Zusammenfassung: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.
Beschreibung:Gesehen am 13.06.2018
Beschreibung:Online Resource
ISSN:1662-5099
DOI:10.3389/fnmol.2017.00214

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