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

Abstract

IntroductionTransmembrane 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 Ca2+ signaling and expression of Ca2+-activated K+ channels. MethodsIonic channel activity was characterized by using whole-cell patch-clamp recording and fura-2 fluorescence. ResultsMean 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 Ca2+-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 Ca2+-activated K+ channels. ConclusionsHuman odontoblasts expressed voltage-dependent Na+ channels, bradykinin receptors, and Ca2+-activated K+ channels, which play an important role in driving cellular functions by channel-receptor signal interaction and membrane potential regulation.