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. 2015 Nov 9;112(47):14711–14716. doi: 10.1073/pnas.1520029112

Fig. 4.

Fig. 4.

Model consistent with imaging, electrophysiological, and biochemical data. (A) CaMKII phosphorylated (P) at Thr286 and PP1 bound to NMDAR-complex; PP1 lacks catalytic access to phospho-CaMKII-T286; in this conformation, NMDAR-complex signaling maintains basal transmission (trace). (B) NMDARcd moves permitting PP1 catalytic access to phospho-CaMKII-T286. (C) CaMKII lacking phosphate on Thr286 is relocated on the NMDARcd, which returns to baseline conformation; CaMKII, along with other signaling molecules activated by metabotropic NMDAR signaling, contributes to synaptic depression (trace). Trace examples taken from Fig. 1A.

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