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Neural Plasticity
Volume 2012 (2012), Article ID 286215, 8 pages
http://dx.doi.org/10.1155/2012/286215
Research Article

GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo

1Bay Zoltán Foundation for Applied Research, BAYGEN, Közép Fasor 41, Szeged 6727, Hungary
2Department of Medical Chemistry, University of Szeged, Szeged, Hungary
3Research Group for Cortical Microcircuits of the Hungarian Academy of Sciences, University of Szeged, Közép Fasor 52, Szeged 6726, Hungary
4Department of Physiology, Anatomy and Neuroscience, University of Szeged, Közép Fasor 52, Szeged 6726, Hungary
5St John’s Collage, University of Oxford, Oxford, UK
6Behavioural & Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK

Received 7 November 2011; Revised 13 January 2012; Accepted 4 February 2012

Academic Editor: Maurizio Popoli

Copyright © 2012 Balázs Barkóczi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

AMPA and NMDA receptors convey fast synaptic transmission in the CNS. Their relative contribution to synaptic output and phosphorylation state regulate synaptic plasticity. The AMPA receptor subunit GluA1 is central in synaptic plasticity. Phosphorylation of GluA1 regulates channel properties and trafficking. The firing rate averaged over several hundred ms is used to monitor cellular input. However, plasticity requires the timing of spiking within a few ms; therefore, it is important to understand how phosphorylation governs these events. Here, we investigate whether the GluA1 phosphorylation (p-GluA1) alters the spiking patterns of CA1 cells in vivo. The antidepressant Tianeptine was used for inducing p-GluA1, which resulted in enhanced AMPA-evoked spiking. By comparing the spiking patterns of AMPA-evoked activity with matched firing rates, we show that the spike-trains after Tianeptine application show characteristic features, distinguishing from spike-trains triggered by strong AMPA stimulation. The interspike-interval distributions are different between the two groups, suggesting that neuronal output may differ when new inputs are activated compared to increasing the gain of previously activated receptors. Furthermore, we also show that NMDA evokes spiking with different patterns to AMPA spike-trains. These results support the role of the modulation of NMDAR/AMPAR ratio and p-GluA1 in plasticity and temporal coding.