Neither CaMKII nor MEK inhibitors modulate KCl-induced pRII increases . (A and B) Effect of the CaMKII inhibitor KN93 (compound effect: F_1,42 = 16.3, P < 0.0003) and its inactive analogue KN-92 (compound effect: F_1,42 = 17, P < 0.0002; 10 µM each, 30-min pretreatment) on the pRII increase induced by KCl (40 mM). (C) Exposure to AIP (1 µM, 30 min) is not inhibiting the pRII response to KCl (40 mM). (D) Exposure to the ERK1/2 inhibitor U0126 (1 µM, 30 min) is not inhibiting the pRII response to KCl (40 mM). (E) Dose–response of KCl (0–80 mM) in the absence or presence of U0126 (1 µM, 30 min). (F) The MEK inhibitor U0126 (1 µM, 30 min) prevents the pERK1/2 increase after KCl depolarization. Values represent means ± SEM; n = 3–4 experiments; >2,000 neurons/condition; two-way ANOVA with Bonferroni’s test; §, P < 0.05; §§§, P < 0.001 indicate significance levels between KCl-induced pRII signals in the absence or presence of an inhibitor.