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. 2013 Jan 7;591(Pt 7):1707–1730. doi: 10.1113/jphysiol.2012.245787

Figure 5. PDE1 is critical for the CaMKII-mediated gating of LTD.

Figure 5

A, signalling components sensitive to the CaMKII activity highlighted by simulation analysis. The CaMKII activity was arbitrarily altered from 0.001 to 10 μm, and the activity level of other signalling molecules were calculated. Highlighted components exhibited large activity changes when the CaMKII activity was altered between 0.1 and 1 μm. The colour indicates the magnitude of activity changes: magenta, >1000%; red, >100%; orange >20%. B and C, simulated time courses of active PP-2A (B) and active PDE1 (C) in response to the LTD induction by the [Ca2+]i increase and glutamate stimulation, in the presence of various amounts of CaMKII. D, simulated time courses of non-phosphorylated AMPARs before and after the LTD induction with or without reduction of the amount of PDE1 in addition to CaMKII reduction. E, time courses of glutamate response amplitudes (n = 5 for each) before and after the LTD stimulation with AIPII and 8-MM-IBMX. Data without (control) and those with AIPII (AIPII, same as those in Fig. 2B) are presented for comparison. Representative current traces in the presence of both AIPII and 8-MM-IBMX are shown in insets.