Microphonic and DPOAE measurements suggest a micromechanical mechanism for the 'bounce' phenomenon following low-frequency tones.

Neural auditory thresholds in the guinea pig can be temporarily improved by up to 6 dB about 2 min after the cessation of an moderately intense low-frequency tone (Kirk and Patuzzi, 1997). We have measured changes in the f2-f1 distortion product otoacoustic emission (DPOAE) and low-frequency microphonic potential in scala tympani before, during and after a low-frequency tone (200 Hz) to determine the cause of this so-called bounce phenomenon. In particular we have analysed the low-frequency microphonic waveform in detail to estimate changes in the maximal receptor current through the outer hair cells (OHCs), the sensitivity of the OHC forward transduction process and the change in OHC operating point on the mechano-electrical transduction transfer curve. Our results indicate that a 200 Hz tone changes the maximal current and sensitivity of the OHCs minimally, but more importantly, it transiently changes the operating point on the OHC transfer curve. In particular, the operating point changes are consistent with a movement of the OHC stereocilia away from the OHC basal body at the peak of the bounce. These changes detected using the microphonic potential are associated with changes in the level of the f2-f1 DPOAE that correlate well with the electrical measurements. We suggest that the shift in operating point is largely responsible for the increase in cochlear sensitivity, and is due to a disruption of the salt balance within the cochlea during the intense low-frequency tone.