Abstract
Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
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Acknowledgements
We thank F.A. Stephenson for providing antibodies to NR1 subunit, R.L. Huganir for providing antibodies to GluR1 subunit, C. Breillat, B. Teissier and D. Bouchet for technical assistance, and G. Marsicano and F. Georges for critical reading of the manuscript. This work was supported by grants from the Centre National de la Recherche Scientifique, Conseil Régional d'Aquitaine, Ministère de la Recherche, Institut National de la Santé et de la Recherche Médicale, Fondation pour la Recherche Médicale, the Human Frontier Science Organization and Agence Nationale de la Recherche.
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L.G. and F.C. developed and supervised the project and conducted the experiments. L.G., D.C. and F.C. wrote the manuscript. L.G. conducted the data analyses.
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Groc, L., Choquet, D. & Chaouloff, F. The stress hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation. Nat Neurosci 11, 868â870 (2008). https://doi.org/10.1038/nn.2150
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DOI: https://doi.org/10.1038/nn.2150
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