CaMKII triggers the diffusional trapping of surface AMPARs through phosphorylation of stargazin

Patricio Opazo, Simon Labrecque, Cezar M. Tigaret, Arnaud Frouin, Paul W. Wiseman, Paul De Koninck, Daniel Choquet
Neuron. 2010-07-01; 67(2): 239-252
DOI: 10.1016/j.neuron.2010.06.007

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Opazo P(1), Labrecque S, Tigaret CM, Frouin A, Wiseman PW, De Koninck P, Choquet

Author information:
(1)CNRS UMR 5091, Cellular Physiology of the Synapse, Bordeaux, France.

The Ca(2+)/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 Ca(2+) influx in the post-synapse triggers a CaMKII- and
Stargazin-dependent decrease in AMPAR diffusional exchange at synapses that
controls synaptic function.


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