Potassium currents in vestibular type II hair cells activated by hydrostatic pressure.
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Abstrakt
An elevated hydrostatic pressure in the endolymphatic space of the inner ear is discussed as pathophysiological factor in hydrops-related diseases of the inner ear. An increase in pressure by fractions of 1 cm H(2)O is sufficient to induce vertigo-like symptoms in animal models. To establish a link between hydrostatic pressure and the function of vestibular hair cells, we studied potassium currents in isolated vestibular type II hair cells from guinea-pig utricles when the hydrostatic pressure was increased by raising the height of the bath from 0.2-0.5, 0.7 or 1.0 cm. Elevated pressure enhanced K(+) currents significantly; a rise in pressure from 0.2-0.5 cm H(2)O increased the total K(+) current at +40 mV by 22+/-14% (+/-S.D.). The pressure-sensitive current I(K,p) was non-inactivating during depolarizing pulses. It was maintained when the pressure was kept elevated for several minutes and receded promptly after return to a pressure of 0.2 cm H(2)O. Voltage-gated Ca(2+) currents, in contrast, were not altered by hydrostatic pressure. A pharmacological characterization of I(K,p) revealed that tetraetylammonium (100 mM) abolished all outward currents including I(K,p). I(K,p) was partly and reversibly inhibited by 4-aminopyridine. Dihydrostreptomycin, a blocker of the transduction channel, left I(K,p) unaffected. Charybdotoxin (100 nM), a blocker of Ca(2+)-dependent K(+) channels, completely yet reversibly abolished I(K,p). We conclude that small elevations in hydrostatic pressure evoke a charybdotoxin-sensitive, probably Ca(2+)-dependent K(+) current in vestibular hair cells. This is likely to alter their frequency response and may be a relevant mechanism how hydrostatic pressure disturbs transduction.