title: Voltage-dependent sodium channels and calcium-activated potassium channels in human odontoblasts in vitro.
abstract: BACKGROUND
  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.
authors.affiliation: Department of Physiology, Tokyo Dental College, Chiba, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Ichikawa
authors.forename: Hyong-Jung
authors.initials: HJ
authors.lastname: Kim
authors.forename: Apichai
authors.initials: A
authors.lastname: Shuprisha
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Shikano
authors.forename: Maki
authors.initials: M
authors.lastname: Tsumura
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Shibukawa
authors.forename: Masakazu
authors.initials: M
authors.lastname: Tazaki
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000704:Analysis of Variance; D001920:Bradykinin / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002461:Cell Line, Transformed; D003782:Dental Pulp / Q000166:cytology*; D016257:Fura-2 / Q000737:chemistry / Q000494:pharmacology; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology; D009804:Odontoblasts / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D024681:Potassium Channels, Calcium-Activated / Q000096:biosynthesis / Q000502:physiology*; D024661:Potassium Channels, Inwardly Rectifying / Q000502:physiology; D018002:Receptors, Bradykinin / Q000378:metabolism; D013997:Time Factors; D061566:Voltage-Gated Sodium Channels / Q000502:physiology*
chemical_list: D024681:Potassium Channels, Calcium-Activated; D024661:Potassium Channels, Inwardly Rectifying; D018002:Receptors, Bradykinin; D061566:Voltage-Gated Sodium Channels; D001920:Bradykinin; D016257:Fura-2