期刊
EMBO JOURNAL
卷 32, 期 4, 页码 496-510出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/emboj.2012.334
关键词
CaMKII; glutamate receptors; hippocampal mossy fibres; kainate receptors; plasticity
资金
- Centre National de la Recherche Scientifique
- Conseil Regional d'Aquitaine
- European Commission [LSHM-CT-2005-019055]
- European Commission (ERC) [232942 Nano-Dyn-Syn]
- Agence Nationale de la Recherche
Calmodulin-dependent kinase II (CaMKII) is key for long-term potentiation of synaptic AMPA receptors. Whether CaMKII is involved in activity-dependent plasticity of other ionotropic glutamate receptors is unknown. We show that repeated pairing of pre- and postsynaptic stimulation at hippocampal mossy fibre synapses induces long-term depression of kainate receptor (KAR)-mediated responses, which depends on Ca2+ influx, activation of CaMKII, and on the GluK5 subunit of KARs. CaMKII phosphorylation of three residues in the C-terminal domain of GluK5 subunit markedly increases lateral mobility of KARs, possibly by decreasing the binding of GluK5 to PSD-95. CaMKII activation also promotes surface expression of KARs at extrasynaptic sites, but concomitantly decreases its synaptic content. Using a molecular replacement strategy, we demonstrate that the direct phosphorylation of GluK5 by CaMKII is necessary for KAR-LTD. We propose that CaMKII-dependent phosphorylation of GluK5 is responsible for synaptic depression by untrapping of KARs from the PSD and increased diffusion away from synaptic sites. The EMBO Journal (2013) 32, 496-510. doi: 10.1038/emboj.2012.334; Published online 4 January 2013
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