External barium influences the gating charge movement of Shaker potassium channels

• Published in: Biophysical journal 1997, Vol.72 (1), p.77-84
• Main Authors: Hurst, R.S., Roux, M.J., Toro, L., Stefani, E.
• Format: Article
• Language: English
• Subjects: Animals; Barium - pharmacology; Female; In Vitro Techniques; Ion Channel Gating - drug effects; Kinetics; Life Sciences; Membrane Potentials - drug effects; Models, Biological; Neurons and Cognition; Oocytes - physiology; Patch-Clamp Techniques; Potassium Channels - drug effects; Potassium Channels - physiology; Recombinant Proteins - drug effects; Recombinant Proteins - metabolism; Sequence Deletion; Shaker Superfamily of Potassium Channels; Xenopus laevis
• ISSN: 0006-3495; 1542-0086
• DOI: 10.1016/S0006-3495(97)78648-X

External Ba2+ speeds the OFF gating currents (IgOFF) of Shaker K+ channels but only upon repolarization from potentials that are expected to open the channel pore. To study this effect we used a nonconducting and noninactivating mutant of the Shaker K+ channel, ShH4-IR (W434F). External Ba2+ slightly decreases the quantity of ON gating charge (QON) upon depolarization to potentials near -30 mV but has little effect on the quantity of charge upon stepping to more hyperpolarized or depolarized potentials. More strikingly, Ba2+ significantly increases the decay rate of IgOFF upon repolarization to -90 mV from potentials positive to approximately -55 mV. For Ba2+ to have this effect, the depolarizing command must be maintained for a duration that is dependent on the depolarizing potential (> 4 ms at -30 mV and > 1 ms at 0 mV). The actions of Ba2+ on the gating current are dose-dependent (EC50 approximately 0.2 mM) and are not produced by either Ca2+ or Mg2+ (2 mM). The results suggest that Ba2+ binds to a specific site on the Shaker K+ channel that destabilizes the open conformation and thus facilitates the return of gating charge upon repolarization.