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

The cochlea of the mustached bat is adapted to process ultrasonic echolocat ion signals. To assess the involvement of active sound amplification by out er hair cells in high-frequency hearing and in audio-vocal interaction, sel ective hair cell damage was induced by the antibiotic Amikacin. Amikacin pr eferentially damaged the first row of outer hair cells in the basal cochlea r turn. The cochlear regions coding for the second-harmonic constant-freque ncy; 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 in crease of mechanical thresholds obtained by measuring distortion-product ot oacoustic emissions. During initial periods of minor hair cell damage, when thresholds had deteriorated by less than 40 dB, a sharp, mechanical, cochl ear resonance that is responsible for enhanced tuning to 61 kHz was still m easurable as a stimulus-frequency otoacoustic emission and its frequency de creased by 350 Hz. The persistence of the resonance suggests that passive s tructures like the tectorial or basilar membrane are important for generati on of the resonance. Behaviorally, the bats reacted to the change in cochle ar micromechanics with a decrease of their CF2 frequency by 360 Hz. After l arger hair cell damage, when the cochlear resonance had disappeared, the ba ts vocalized only sparsely and the CF2 frequency increased by up to 2 kHz, which may correspond to a state without audio-vocal feedback. This indicate s that audio-vocal feedback in the nondamaged animal works to lower the cal l frequency.