Abstract

Vestibular type II hair cells respond to increases in the hydrostatic pressure with pressure-dependent K(+) currents. We examined whether such currents may modulate transmitter release (assessed as membrane capacitance increments) by altering membrane potentials and voltage-gated Ca(2+) currents. Capacitance increments were dependent on voltage-gated Ca(2+) influx. Stimulating currents (0.7 nA) in current clamp induced depolarisations that were more negative by 8.7 +/- 2.1 mV when the bath height was elevated from 0.2 to 0.5 cm. In voltage clamp, protocols were used that simulated the time course of the membrane potential in current clamp at either low (control) or high hydrostatic pressure (high bath). The low bath protocol induced significantly larger Ca(2+) currents and increases in capacitance than the high bath protocol. We conclude that pressure-dependent K(+) currents may alter the voltage response of vestibular hair cells to an extent critical for Ca(2+) currents and transmitter release. This mechanism may contribute to vestibular dysfunction in Meniere's disease.

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