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. 2021 Dec 15;10:e60360. doi: 10.7554/eLife.60360

Figure 2. Ca2+-calmodulin-dependent kinase II (CaMKII) inhibitor AIP inhibits AMPAR synaptic transmission through CaMKIIα.

Figure 2.

(A) In culture slices, transfection of AIP reduced AMPAR EPSCs (left, n = 10, p < 0.01, two-tailed Wilcoxon Signed Rank Test) but not NMDAR EPSCs (right, n = 10, p > 0.05, two-tailed Wilcoxon Signed Rank Test). Sample traces show the effects of AIP on AMPAR EPSCs and NMDAR EPSCs. (B) AMPA/NMDA ratios compared to wild-type (WT) (n = 34) are reduced after myr-AIP (20 µM) treatment (n = 12). Scale bar = 50 pA vertical and 30 ms horizontal. (C) Left, summary of the effect of myr-AIP (20 µM) on AMPAR EPSCs in wt cells (n = 6) and interleaved CRISPR-CaMKIIα transfected cells (n = 5) from culture slices, normalized to each cell’s baseline. The difference between control and CRISPR-CaMKIIα transfected cells at 30 min: p < 0.01, Mann–Whitney U test. Right, sample traces showing myr-AIP inhibition of AMPAR EPSC in control cells, but not in CRISPR-CaMKIIα transfected cells. Black traces are control cell, green are transfected cell. Mean ± standard error of the mean (SEM).

Figure 2—source data 1. Ca2+-calmodulin-dependent kinase II (CaMKII) inhibitor AIP inhibits AMPAR synaptic transmission through CaMKIIα.
In this dataset, the results of the effects of AIP on AMPAR EPSCs and NMDAR EPSCs are included.