Low cytoplasmic [Ca2+] activates I-CRAC independently of global Ca2+ storedepletion in RBL-1 cells

Release of Ca2+ from inositol (1,4,5)-trisphosphate-sensitive Ca2+ stores c auses "capacitative calcium entry," which is mediated by the so-called "Ca2 + release-activated Ca2+ current" (I-CRAC) in RBL-1 cells. Refilling of the Ca2+ stores or high cytoplasmic [Ca2+] ([Ca2+](cyt)) inactivate I-CRAC. He re we address the question if also [Ca2+](cyt) lower than the resting [Ca2](cyt) influences store operated channels. We therefore combined patch clam p and mag fura-2 fluorescence methods to determine simultaneously both I-CR AC and [Ca2+] within Ca2+ stores of RBL-1 cells ([Ca2+](store)). We found t hat low [Ca2+](cyt) in the range of 30-50 nM activates I-CRAC and Ca2+ infl ux spontaneously and independently of global Ca2+ store depletion, while el evation of [Ca2+](cyt) to the resting [Ca2+](cyt) (100 nM) resulted in stor e dependence of I-CRAC activation. We conclude that spontaneous activation of I-CRAC by low [Ca2+](cyt) could serve as a feedback mechanism keeping th e resting [Ca2+](cyt) constant.