Store-operated Ca2+ entry in fetal skeletal muscle cells. (A) High-K+ bath solution did not trigger intracellular Ca2+ release in an E16 cell preincubated in 0 Ca2+ for ∼2 h. Perfusion of 2 mM Ca2+ led to sustained elevation of cytosolic [Ca2+]i. No further increase was observed when [Ca2+]o was applied for the second time. Second exposure to high-K+ triggered transient elevation of [Ca2+]i, indicative of SR Ca2+ refilling. (B) The cell was pretreated with thapsigargin (10 μM) for 10 min. Switching the bath solution from 0 Ca2+ to 2 mM Ca2+ led to elevation of [Ca2+]i via SOCE, which was inhibited by 2-APB. (C) Quenching of Fura-2 fluorescence by 0.5 mM Mn2+ in a cell with passively depleted SR Ca2+ content. 5 μM nifedipine did not affect the rate of Fura-2 quenching. (D) Mn2+ quenching of Fura-2 measured in the same cell, in the control condition with passively depleted SR Ca2+ content, after addition of 10 μM thapsigargin, and after addition of 20 μM 2-APB. (E) Mn2+ entry rate was reversibly and reproducibly decreased when the bath solution was changed from control to a high-K+ solution.