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First published online February 18, 2009
doi: 10.1242/10.1242/jcs.037382

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The function of glutamatergic synapses is not perturbed by severe knockdown of 4.1N and 4.1G expression

Christian Wozny^1,*,,, Jörg Breustedt^1,*, Friederike Wolk^2,*, Frédérique Varoqueaux², Susann Boretius³, Aleksandar R. Zivkovic¹, Antje Neeb⁴, Jens Frahm³, Dietmar Schmitz¹, Nils Brose² and Aleksandra Ivanovic^2,

¹ Neuroscience Research Center, Charité–Universitätsmedizin Berlin, Charitéplatz 1, D-10117 Berlin, Germany
² Max-Planck-Institut für Experimentelle Medizin, Abteilung Molekulare Neurobiologie, DFG Center for Molecular Physiology of the Brain, Hermann-Rein-Str. 3, D-37075 Göttingen, Germany
³ Biomedizinische NMR Forschungs GmbH, Max-Planck-Institut für Biophysikalische Chemie, Am Fassberg 11, D-37077 Göttingen, Germany
⁴ Institut für Toxikologie und Genetik, Forschungszentrum Karlsruhe, Hermann-von-Helmholtz-Platz 1, D-76344 Eggenstein-Leopoldshafen, Germany

Authors for correspondence (e-mails: ivanovic{at}em.mpg.de; cwozny{at}mrc-lmb.cam.ac.uk)

Accepted 6 November 2008

AMPA-type glutamate receptors mediate fast excitatory synaptic transmission in the vertebrate brain. Their surface expression at synapses between neurons is regulated in an activity-dependent and activity-independent manner. The protein machinery that regulates synaptic targeting, anchoring and turnover of AMPA receptors consists of several types of specialized scaffolding proteins. The FERM domain scaffolding proteins 4.1G and 4.1N were previously suggested to act jointly in binding and regulating synaptic trafficking of the AMPA receptor subunits GluR1 and GluR4. To determine the functions of 4.1G and 4.1N in vivo, we generated a mutant mouse line that lacks 4.1G entirely and expresses 4.1N at 22% of wild-type levels. These mice had combined 4.1G and 4.1N protein expression in the hippocampus at 12% of wild-type levels (equivalent to 8-10% of combined GluR1 and GluR4 expression levels). They show a moderate reduction in synaptosomal expression levels of the AMPA receptor subunit GluR1 at 3 weeks of age, but no change in basic glutamatergic synaptic transmission and long-term potentiation in the hippocampus. Our study indicates that 4.1G and 4.1N do not have a crucial role in glutamatergic synaptic transmission and the induction and maintenance of long-term plastic changes in synaptic efficacy.

Key words: Knockout, Mouse, Hippocampus, GluR1, GluR4, Synaptic plasticity

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