Inwardly rectifying potassium currents in rat basophilic leukaemia (RBL-1) cells: regulation by spermine and implications for store-operated calcium influx

Abstract.

In non-excitable cells, the major Ca²⁺ influx pathway is the store-operated one. Store-operated Ca²⁺ entry is intimately related to the prevalent membrane potential, in that hyperpolarisation enhances Ca²⁺ 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 Ca²⁺ 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 Ca²⁺ 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 [Ca²⁺] 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 Ca²⁺ influx is discussed.