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. 2022 Jun 13;33(1):e13099. doi: 10.1111/bpa.13099

FIGURE 6.

FIGURE 6

R1‐Pep did not affect CaMKII expression but stress‐induced CaMKII(T286) autophosphorylation. (A, B) Glutamate‐stressed neurons were treated for 16 h with R1‐Pep (10 μg/ml) or R1‐Pep plus the GABAB receptor antagonist CGP 56999 (10 μM) and then analyzed by Western blotting using antibodies directed against α, β, γ, and δ subtypes of CaMKII (A) or specifically to CaMKIIβ (B). Signals were normalized to control. N = 12 (A) or 8 (B) cultures per condition from four (A) and three (B) independent preparations, respectively. One‐way ANOVA with Tukey's multiple comparison test (ns, p > 0.05). (C) R1‐Pep inhibited glutamate stress‐induced T286 autophosphorylation of CaMKII. Glutamate‐stressed neurons were treated for 16 h with R1‐Pep (10 μg/ml) or R1‐Pep plus the GABAB receptor antagonist CGP 56999 and then analyzed by Western blotting using antibodies directed against pCaMKII(T286). Signals were normalized to control. N = 11 cultures per condition from four independent preparations. Two‐way ANOVA with Dunnett's T3 multiple comparison test (ns, p > 0.05; *, p < 0.05; **, p < 0.01).