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GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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 tr...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3337492/ https://www.ncbi.nlm.nih.gov/pubmed/22567428 http://dx.doi.org/10.1155/2012/286215 |
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author | Barkóczi, Balázs Juhász, Gábor Averkin, Robert G. Vörös, Imre Vertes, Petra Penke, Botond Szegedi, Viktor |
author_facet | Barkóczi, Balázs Juhász, Gábor Averkin, Robert G. Vörös, Imre Vertes, Petra Penke, Botond Szegedi, Viktor |
author_sort | Barkóczi, Balázs |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3337492 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-33374922012-05-07 GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo Barkóczi, Balázs Juhász, Gábor Averkin, Robert G. Vörös, Imre Vertes, Petra Penke, Botond Szegedi, Viktor Neural Plast Research Article 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. Hindawi Publishing Corporation 2012 2012-04-09 /pmc/articles/PMC3337492/ /pubmed/22567428 http://dx.doi.org/10.1155/2012/286215 Text en Copyright © 2012 Balázs Barkóczi et al. https://creativecommons.org/licenses/by/3.0/ 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. |
spellingShingle | Research Article Barkóczi, Balázs Juhász, Gábor Averkin, Robert G. Vörös, Imre Vertes, Petra Penke, Botond Szegedi, Viktor GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo |
title | GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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title_full | GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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title_fullStr | GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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title_full_unstemmed | GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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title_short | GluA1 Phosphorylation Alters Evoked Firing Pattern In Vivo
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title_sort | glua1 phosphorylation alters evoked firing pattern in vivo |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3337492/ https://www.ncbi.nlm.nih.gov/pubmed/22567428 http://dx.doi.org/10.1155/2012/286215 |
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