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. Author manuscript; available in PMC: 2012 Jun 1.
Published in final edited form as: Neuroscientist. 2011 Apr 15;17(3):321–336. doi: 10.1177/1073858410384740

Figure 3. The AKAP79/150-MAGUK postsynaptic signaling complex in regulation of AMPA receptor phosphorylation during synaptic plasticity.

Figure 3

A) AKAP79/150 can be linked to both AMPA and NMDA receptors through MAGUK scaffolding proteins. Influx of Ca2+ through the NMDAR activates CaN, PKC, and PKA activity to regulate postsynaptic substrate phosphorylation including AMPAR-GluR1. B) Regulation of the AMPAR endocytosis and translocation of AKAP79/150 from the PSD during LTD. Ca2+ influx through the NMDAR activates AKAP-anchored CaN, resulting in dephosphorylation of the GluR1-Ser845 and AMPAR endocytosis. Activation of CaN along with PLC also promotes depolymerization of spine actin to promote subsequent translocation of AKAP-PKA complexes away from the postsynaptic membrane in dendritic spines. This delayed movement of AKAP79/150-PKA away from spines may prevent re-phosphorylation and recycling of AMPARs during LTD.