Consequences of outer hair cell damage for otoacoustic emissions and audio-vocal feedback in the mustached bat.

Abstract

The cochlea of the mustached bat is adapted to process ultrasonic echolocation signals. To assess the involvement of active sound amplification by outer hair cells in high-frequency hearing and in audio-vocal interaction, selective hair cell damage was induced by the antibiotic Amikacin. Amikacin preferentially damaged the first row of outer hair cells in the basal cochlear turn. The cochlear regions coding for the second-harmonic constant-frequency component of the echolocation call (CF2) at 61 kHz and for frequencies between 75 and 100 kHz were the most affected. This was reflected in an increase of mechanical thresholds obtained by measuring distortion-product otoacoustic emissions. During initial periods of minor hair cell damage, when thresholds had deteriorated by less than 40 dB, a sharp, mechanical, cochlear resonance that is responsible for enhanced tuning to 61 kHz was still measurable as a stimulus-frequency otoacoustic emission and its frequency decreased by 350 Hz. The persistence of the resonance suggests that passive structures like the tectorial or basilar membrane are important for generation of the resonance. Behaviorally, the bats reacted to the change in cochlear micromechanics with a decrease of their CF2 frequency by 360 Hz. After larger hair cell damage, when the cochlear resonance had disappeared, the bats vocalized only sparsely and the CF2 frequency increased by up to 2 kHz, which may correspond to a state without audiovocal feedback. This indicates that audio-vocal feedback in the nondamaged animal works to lower the call frequency.