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In non-excitable cells, the major Ca(2+) influx pathway is the store-operated one. Store-operated Ca(2+) entry is intimately related to the prevalent membrane potential, in that hyperpolarisation enhances Ca(2+) influx and depolarisation reduces it. Inwardly rectifying potassium channels are important determinants of the membrane potential and hence will regulate, indirectly, the rate and extent of Ca(2+) entry through store-operated channels. Here we investigated inwardly rectifying potassium currents ( I(RK)) in rat basophilic leukaemia (RBL-1) cells, a model system for studying store-operated Ca(2+) influx. I(RK) was voltage dependent in that the current decays during strong hyperpolarisations. Recovery from this decay was both time and voltage dependent. Close to the resting potential of RBL-1 cells, however, I(RK) was stable. Neither store depletion per se nor the subsequent rise in intracellular [Ca(2+)] appeared to alter I(RK) activity. Receptor stimulation reduced the current only weakly. Unexpectedly, intracellular spermine inhibited I(RK) quite strongly and via a mechanism that seemed distinct from that responsible for current rectification. The relevance of these findings to store-operated Ca(2+) influx is discussed.

Original publication




Journal article


Pflugers Arch

Publication Date





389 - 396


Animals, Calcium, Carbachol, Cholinergic Agonists, Ion Channel Gating, Leukemia, Basophilic, Acute, Membrane Potentials, Patch-Clamp Techniques, Potassium, Potassium Channels, Inwardly Rectifying, Rats, Spermine, Stimulation, Chemical, Tumor Cells, Cultured