Opazo, Patricio, Labrecque, Simon, Tigaret, Cezar M. ![]() |
Abstract
The Ca2+/calmodulin-dependent protein kinase II (CaMKII) is critically required for the synaptic recruitment of AMPA-type glutamate receptors (AMPARs) during both development and plasticity. However, the underlying mechanism is unknown. Using single-particle tracking of AMPARs, we show that CaMKII activation and postsynaptic translocation induce the synaptic trapping of AMPARs diffusing in the membrane. AMPAR immobilization requires both phosphorylation of the auxiliary subunit Stargazin and its binding to PDZ domain scaffolds. It does not depend on the PDZ binding domain of GluA1 AMPAR subunit nor its phosphorylation at Ser831. Finally, CaMKII-dependent AMPAR immobilization regulates short-term plasticity. Thus, NMDA-dependent Ca2+ influx in the post-synapse triggers a CaMKII- and Stargazin-dependent decrease in AMPAR diffusional exchange at synapses that controls synaptic function.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine Neuroscience and Mental Health Research Institute (NMHRI) |
Publisher: | Elsevier (Cell Press) |
ISSN: | 0896-6273 |
Date of First Compliant Deposit: | 14 January 2020 |
Date of Acceptance: | 3 June 2010 |
Last Modified: | 26 Oct 2022 08:52 |
URI: | https://orca.cardiff.ac.uk/id/eprint/128524 |
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