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. Author manuscript; available in PMC: 2010 Dec 27.
Published in final edited form as: Physiology (Bethesda). 2010 Feb;25(1):41–49. doi: 10.1152/physiol.00033.2009

FIGURE 3. A model for the regulation of AMPAR localization.

FIGURE 3

Neuronal activity increases calcium influx through NMDAR to activate calcium-dependent kinases, which is followed by an increase in AMPARs at synapses. TARPs are highly phosphorylated at the PSD. TARP is a substrate of PKC and CaMKII in vitro. These observations indicate that TARP phosphorylation is a regulator of synaptic AMPAR activity and may be a substrate for NMDAR-mediated synaptic plasticity.