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

Figure 1. Ca2+-calmodulin-dependent kinase II (CaMKII) inhibitor myr-CN27 inhibits AMPAR synaptic transmission through CaMKIIα.

(A) Time course of myr-CN27 (1 µM) inhibition on AMPAR EPSCs and NMDAR EPSCs in acute slices. (B) Summary graphs showing myr-CN27 inhibited AMPAR EPSCs (before drug: 63.9 ± 12 pA; after drug: 27.6 ± 3.9 pA; n = 10, p < 0.01, two-tailed Wilcoxon Signed Rank Test), but not NMDAR EPSCs (before drug: 43.2 ± 13.7 pA; after drug: 42 ± 13.4 pA; n = 5, p > 0.05, two-tailed Wilcoxon Signed Rank Test). (C) Time course of the effect of myr-CN27 on AMPAR EPSCs in wt cells and simultaneously recorded CRISPR-CaMKIIα transfected cells, normalized to wt baseline (from culture slices). While myr-CN27 inhibited AMPAR EPSCs in wt cells, it had no effect on CRISPR-CaMKIIα transfected cells (n = 6, p > 0.05, two-tailed Wilcoxon Signed Rank Test). (D) Sample traces showing that myr-CN27 inhibited AMPAR EPSCs in control cells, but had no effect in CRISPR-CaMKIIα transfected cells. Black traces are control cell, green traces are transfected cell. Mean ± standard error of the mean (SEM). **p < 0.01. (E) A comparison of the reduction of synaptic transmission in field and whole cell recording. For the field recording (black, n = 8) after a 60-min stable baseline, 1 μM myr-CN27 was applied to the slice for 100 min. For the whole cell recording (blue, n = 7), the drug was applied after a 10-min stable baseline. In both, the response was reduced to 50% of baseline. Example traces for both are shown taken at the timepoints indicated by 1 and 2. The field EPSPs shown on the bottom right have scale bars vertical 0.1 mV and 5 ms horizontal. The whole cell recording shown bottom left have scale bars 50 pA vertical and 20 ms horizontal. Both recordings are done in WT slices with the whole cell recordings done in slice culture DIV3–14 while the fields were done in acute slices from P15–28 mice.

Figure 1—source data 1. Ca2+-calmodulin-dependent kinase II (CaMKII) inhibitor myr-CN27 inhibits AMPAR synaptic transmission through CaMKIIα.
In this dataset, the results of the effects of myr-CN27 on AMPAR EPSCs and NMDAR EPSCs are included.

Figure 1.

Figure 1—figure supplement 1. The effect of various Ca2+-calmodulin-dependent kinase II (CaMKII) peptide inhibitors on the AMPAR/NMDAR ratio.

Figure 1—figure supplement 1.

AMPAR/NMDAR ratios recorded in acute slices made from wild-type (WT) mice incubated without inhibitor treatment (WT) (n = 34), with 5 μM tatCN21 (n = 10), with 1 μM myr-CN27 (n = 47), and with 5 μM myr-CN21 (n = 9). Sample traces are shown at top. Scale bar = 50 pA vertical and 30 ms horizontal p < 0.01, Mann–Whitney U test.