Abstract

Event Abstract Back to Event Analyzing NMDA and AMPA evoked spike-trains in CA1: GluA1 phosphorylation specific patterns in vivo Balázs Barkóczi1*, Gábor Juhász2, Robert Averkin1, Imre Vörös3, Botond Penke1, 2 and Viktor Szegedi1 1 Bay Zoltán Foundation for Applied Research, BAYGEN, Hungary 2 University of Szeged, Department of Medical Chemistry, Faculty of General Medicine, Hungary 3 University of Oxford, St John's College, United Kingdom AMPA and NMDA type glutamate receptors convey fast synaptic transmission in the CNS and mediate various forms of hippocampal plasticity. AMPA receptors comprise four subunits – GluA1, GluA2, GluA3 and GluA4 (or GluR1-4) – that combine to form tetramers. GluA1 is central in synaptic plasticity: disruption of glutamate receptor type 1 causes synaptic alterations and learning/memory deficits in mice. Phosphorylation of serines 831 and 845 in the GluA1 subunit by CaMKII and PKA respectively regulates the ion channel properties and synaptic trafficking of GluR1-containing AMPARs during hippocampal LTP. Moreover, altered phosphorylation pattern of GluA1 was shown in various forms of mental disorders, like addiction, mania and major depressive disorder. Tianeptine, an atypical antidepressant, have been shown to increase the phosphorylation level of GluA1 on the CaMKII and PKA site, resulting in enhanced AMPA-evoked spiking activity in vivo. Here we investigated whether the increased level of GluA1 phosphorylation has a specific “fingerprint” on the AMPA-evoked spiking pattern of single CA1 cell in vivo. AMPA evoked spiking trains were recorded from the CA1 region of chloral-hydrate anaesthetized male rats before and after i.p. Tianeptine application. In another set of experiments, weak and strong AMPA and NMDA-stimulation was applied for evoking spike-trains. By comparing AMPA evoked spike-trains with similar firing rates, we show that the spike-trains recorded after Tianeptine application show characteristic features, distinguishing from spike-trains triggered by strong AMPA stimulation. Despite the similar firing rates, the interspike interval distributions are significantly different among the two groups, showing that neuronal output may differ when new receptors are activated compared to posttranscriptional regulation of previously activated receptors. Furthermore, we also show that NMDA evokes spiking activity with different pattern than AMPA induced spike-trains. Conference: IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010. Presentation Type: Poster Presentation Topic: Disorders of the nervous system Citation: Barkóczi B, Juhász G, Averkin R, Vörös I, Penke B and Szegedi V (2010). Analyzing NMDA and AMPA evoked spike-trains in CA1: GluA1 phosphorylation specific patterns in vivo. Front. Neurosci. Conference Abstract: IBRO International Workshop 2010. doi: 10.3389/conf.fnins.2010.10.00025 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 19 Apr 2010; Published Online: 19 Apr 2010. * Correspondence: Balázs Barkóczi, Bay Zoltán Foundation for Applied Research, BAYGEN, Szeged, Hungary, barkoczib@baygen.hu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Balázs Barkóczi Gábor Juhász Robert Averkin Imre Vörös Botond Penke Viktor Szegedi Google Balázs Barkóczi Gábor Juhász Robert Averkin Imre Vörös Botond Penke Viktor Szegedi Google Scholar Balázs Barkóczi Gábor Juhász Robert Averkin Imre Vörös Botond Penke Viktor Szegedi PubMed Balázs Barkóczi Gábor Juhász Robert Averkin Imre Vörös Botond Penke Viktor Szegedi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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