Figure 3. H₂O₂ induces an increase in mEPSC frequency by modulating Ca²⁺ influx via N‐type VGCCs .

A, effect of H₂O₂ on mEPSCs in Ca²⁺‐free ACSF. Under this condition, the H₂O₂‐induced mEPSC increase but not its subsequent depression was completely blocked. B, summary of mEPSC frequency in Ca²⁺‐free ACSF (mean ± SEM, n = 7). Values in the charts correspond to percentage change in maximal values of mEPSC frequency relative to the control during H₂O₂ superfusion and after washout. The P value was determined by a paired t test. C, ω‐Aga (0.2 μm), a P/Q‐type VGCC blocker, partially suppressed the H₂O₂‐induced increase in mEPSC frequency. D, ω‐Ctx (0.5 μm), an N‐type VGCC blocker, completely suppressed the increase in frequency. E, summary of mEPSC frequencies observed during H₂O₂ superfusion with TTX alone (n = 11) or with nifedipine (L‐type VGCC blocker, 10 μm; n = 7), ω‐Aga (0.2 μm; n = 6), ω‐Ctx (0.5 μm; n = 6), or SNX‐482 (R‐type VGCC blocker, 0.1 μm; n = 6) relative to control (mean ± SEM). Maximal values of mEPSC frequency relative to the control 1.5–6 min after H₂O₂ superfusion are shown. P values were determined by one‐way ANOVA with a Bonferroni post hoc test. The holding potential was −70 mV for all recordings. Washout indicates the 10 min period after initiating H₂O₂ washout.