Figure 4.

Blocking SERCA reproduced abnormal Ca²⁺ dynamics observed in STIM1^PKO mice. A, CPA (30 μm) elevated the level of accumulated Ca²⁺ in wild-type mice to that of STIM1^PKO mice. Under the same firing rate as achieved by AP clamping, Ca²⁺ more rapidly accumulated after CPA treatment (top). At the 30 s point, the changed Ca²⁺ signal ratio of wild-type mice was significantly lower than that of CPA-treated groups and STIM1^PKO mice (wild-type, n = 7; STIM1^PKO, n = 7; wild-type + CPA, n = 7; STIM1^PKO + CPA, n = 8; F = 8.589, p < 0.001, bottom). Lines and shaded areas show the mean and SEM. B, Prolonged decaying τ of Ca²⁺ transient by CPA treatment. Representative traces with fitted single exponential curves (left). Decaying τ became significantly longer in CPA-treated groups (wild-type, n = 15; STIM1^PKO, n = 13; wild-type + CPA, n = 9; STIM1^PKO + CPA, n = 9; F = 14.492, p < 0.001, top right). Peak values were not different among all groups (F = 0.562, p < 0.643, bottom right). Drug-untreated data from wild-type and STIM1^PKO mice were pooled from Figure 1. One-way ANOVA with post hoc Fisher's LSD test for statistics. Error bars denote the SEM. *p < 0.05; ***p < 0.001.