In this paper, we show further evidences for the existence of store-operated calcium entry in differentiated skeletal muscle C2C12 myotubes after Ca2+ depletion in sarcoplasmic reticulum, using thapsigargin, a potent sarcoplasmic reticulum Ca2+-ATPase inhibitor, caffeine as ryanodine receptor activator, and ATP which activates purinergic receptors. The quenching of fura 2 fluorescence emission by Mn2+ also provided evidences for store-operated calcium entry because this quenching was accelerated when sarcoplasmic reticulum was depleted of Ca2+. Ca2+ entry was sensitive to Ni2+, La3+, Gd3+ and 2-aminoethyl diphenyl borate but resistant to nifedipine, thus excluding L-type Ca2+ channels in this type of calcium entry. Our data obtained using ATP for store depletion suggest that the level of Ca2+ in internal stores could play a role in the regulation of store-operated calcium channel activity in this cell type.
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