Voltage-dependent Sodium Channels and Calcium-activated Potassium Channels in Human Odontoblasts In Vitro

Abstract Introduction Transmembrane ionic signaling regulates many cellular processes in both physiological and pathologic settings. In this study, the biophysical properties of voltage-dependent Na + channels in odontoblasts derived from human dental pulp (HOB cells) were investigated together with the effect of bradykinin on intracellular Ca 2+ signaling and expression of Ca 2+ -activated K + channels. Methods Ionic channel activity was characterized by using whole-cell patch-clamp recording and fura-2 fluorescence. Results Mean resting membrane potential in the HOB cells was −38 mV. Depolarizing steps from a holding potential of −80 mV activated transient voltage-dependent inward currents with rapid activation/inactivation properties. At a holding potential of −50 mV, no inward current was recorded. Fast-activation kinetics exhibited dependence on membrane potential, whereas fast-inactivation kinetics did not. Steady-state inactivation was described by a Boltzmann function with a half-maximal inactivation potential of −70 mV, indicating that whereas the channels were completely inactivated at physiological resting membrane potential, they could be activated when the cells were hyperpolarized. Inward currents disappeared in Na + -free extracellular solution. Bradykinin activated intracellular Ca 2+ -releasing and influx pathways. When the HOB cells were clamped at a holding potential of −50 mV, outward currents were recorded at positive potentials, indicating sensitivity to inhibitors of intermediate-conductance Ca 2+ -activated K + channels. Conclusions Human odontoblasts expressed voltage-dependent Na + channels, bradykinin receptors, and Ca 2+ -activated K + channels, which play an important role in driving cellular functions by channel-receptor signal interaction and membrane potential regulation.