Abstract
Ca2+-dependent vesicular fusion was studied in single whole-cell patch-clamped rat basophilic leukemia (RBL) cells using the capacitance technique. Dialysis of the cells with 10 µM free Ca2+ and 300 µM guanosine 5′-O-(3-thiotriphosphate) (GTP[γ-S]) resulted in prominent capacitance increases. However, dialysis with either Ca2+ (225 nM to 10 µM) or GTP[γ-S] alone failed to induce a capacitance change. Under conditions of weak Ca2+ buffering (0.1 mM EGTA), activation of Ca2+-release-activated Ca2+ (CRAC) channels by dialysis with inositol 1,4,5-trisphosphate (InsP 3) failed to induce a capacitance increase even in the presence of GTP[γ-S]. However, when Ca2+ATPases were inhibited by thapsigargin, InsP 3 and GTP[γ-S] led to a pronounced elevation in membrane capacitance. This increase was dependent on a rise in intracellular Ca2+ because it was abolished when cells were dialysed with a high level of EGTA (10 mM) in the recording pipette. The increase was also dependent on Ca2+ influx because it was effectively suppressed when external Ca2+ was removed. Our results demonstrate that I CRAC represents an important source of Ca2+ for triggering a secretory response.
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Received: 1 May 1998 / Received after revision: 15 June 1998 / Accepted: 2 July 1998
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Artalejo, A., Ellory, J. & Parekh, A. Ca2+-dependent capacitance increases in rat basophilic leukemia cells following activation of store-operated Ca2+ entry and dialysis with high-Ca2+-containing intracellular solution. Pflügers Arch 436, 934–939 (1998). https://doi.org/10.1007/PL00008088
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DOI: https://doi.org/10.1007/PL00008088