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Voltage-dependent conductance changes in the store-operated Ca²⁺ current I_CRAC in rat basophilic leukaemia cells

Daniel Bakowski and Anant B. Parekh

1. Tight-seal whole-cell patch-clamp experiments were carried out in order to investigate the effects of different holding potentials on the rate of development and amplitude of the Ca²⁺ release-activated Ca²⁺ current I_CRAC in rat basophilic leukaemia (RBL-1) cells. I_CRAC was monitored at -80 mV from fast voltage ramps, spanning 200 mV in 50 ms.

2. At hyperpolarised potentials, the macroscopic CRAC conductance was lower than that seen at depolarised potentials. The conductance increased almost 5-fold over the voltage range -60 to +40 mV and was seen when the stores were depleted either by the combination of IP₃ and thapsigargin in high Ca²⁺ buffer, or passively with 10 mM EGTA or BAPTA.

3. The voltage-dependent conductance of the CRAC channels could not be fully accounted for by Ca²⁺-dependent fast inactivation, nor by other slower inhibitory mechanisms. It also did not seem to involve intracellular Mg²⁺ or the polycations spermine and spermidine.

4. Voltage step relaxation experiments revealed that the voltage-dependent conductance changes developed and reversed slowly, with a time constant of several seconds at -60 mV.

5. In the presence of physiological levels of intracellular Ca²⁺ buffers, I_CRAC was barely detectable when cells were clamped at -60 mV and dialysed with IP₃ and thapsigargin, but at 0 mV the current in low Ca²⁺ buffer was as large as that seen in high Ca²⁺ buffer.

6. Our results suggest that CRAC channels exhibit slow voltage-dependent conductance changes which can triple the current amplitude over the physiological range of voltages normally encountered by these cells. The role of this conductance change and possible underlying mechanisms are discussed.

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