Slow motility, electromotility and lateral wall stiffness in the isolated outer hair cells.

Slow motile length changes of isolated, apical turn outer hair cells (OHCs) (n=36) were induced by perfusion of saline (flow rate: 0.6 microl/min) as a mechanical challenge or by perfusion of 12.5 mM KCl solution for 90 s as a chemical and mechanical challenge with and without ocadaic acid (OA), a serine/threonine protein phosphatase inhibitor. Electromotility was evoked by square pulses from +/-35 mV to +/-240 mV during the slow shortening and recovery period (n=36). Stiffness of the lateral wall was measured by the micropipette aspiration technique (n=20). Saline perfusion caused a reversible shortening of 774+/-87 nm (n=9) as well as K+ of 1465+/-159 nm (n=9). Slow shortening increased lateral wall stiffness (1.25+/-0.02 to 1.52+/-0.03 nN/microm) (n=5-5). Simultaneously, electromotility magnitude decreased (n=9). Ocadaic acid blocked slow shortening, increased lateral wall stiffness, and decreased the magnitude of electromotility. Mechanical or mechanical+chemical stimulation of ocadaic acid treated OHCs do not further change stiffness or electromotility. Isolated OHCs respond with slow shortening and consutive cell stiffness increase to mechanical insult. This phenomenon seems operating with calcium-, and phosphorylation-dependent modifications of the cytoskeletal proteins. The subsequent electromotility gain decrease suggests a slow OHC shortening driven regulation of the cochlear amplifier with simultaneous safety control of the auditory periphery against overstimulation.