Using the Cochlear Microphonic as a Tool to Evaluate Cochlear Function in Mouse Models of Hearing

The cochlear microphonic (CM) can be a useful analytical tool, but many investigators may not be fully familiar with its unique properties to interpret it accurately in mouse models of hearing. The purpose of this report is to develop a model for generation of the CM in wild-type (WT) and prestin knockout mice. Data and modeling results indicate that in the majority of cases, the CM is a passive response, and in the absence of outer hair cell (OHC) damage, mice lacking amplification are expected to generate WT levels of CM for inputs less than ~30 kHz. Hence, this cochlear potential is not a useful metric to estimate changes in amplifier gain. This modeling analysis may explain much of the paradoxical data in the literature. For example, various manipulations, including the application of salicylate and activation of the crossed olivocochlear bundle, reduce the compound action potential but increase or do not change the CM. Based on this current evaluation, CM measurements are consistent with early descriptions where this AC cochlear potential is dominated by basal OHCs, when recorded at the round window

Stereocilin-deficient mice reveal the origin of cochlear waveform distortions

Although the cochlea is an amplifier and a remarkably sensitive and finely tuned detector of sounds, it also produces conspicuous mechanical and electrical waveform distortions. These distortions reflect nonlinear mechanical interactions within the cochlea. By allowing one tone to suppress another (masking effect), they contribute to speech intelligibility. Tones can also combine to produce sounds with frequencies not present in the acoustic stimulus. These sounds compose the otoacoustic emissions that are extensively used to screen hearing in newborns. Because both cochlear amplification and distortion originate from the outer hair cells-one of the two types of sensory receptor cells-it has been speculated that they stem from a common mechanism. Here we show that the nonlinearity underlying cochlear waveform distortions relies on the presence of stereocilin, a protein defective in a recessive form of human deafness. Stereocilin was detected in association with horizontal top connectors, lateral links that join adjacent stereocilia within the outer hair cell's hair bundle. These links were absent in stereocilin-null mutant mice, which became progressively deaf. At the onset of hearing, however, their cochlear sensitivity and frequency tuning were almost normal, although masking was much reduced and both acoustic and electrical waveform distortions were completely lacking. From this unique functional situation, we conclude that the main source of cochlear waveform distortions is a deflection-dependent hair bundle stiffness resulting from constraints imposed by the horizontal top connectors, and not from the intrinsic nonlinear behaviour of the mechanoelectrical transducer channel

Evoked cochlear potentials in the barn owl

Gross electrical responses to tone bursts were measured in adult barn owls, using a single-ended wire electrode placed onto the round window. Cochlear microphonic (CM) and compound action potential (CAP) responses were evaluated separately. Both potentials were physiologically vulnerable. Selective abolishment of neural responses at high frequencies confirmed that the CAP was of neural origin, while the CM remained unaffected. CAP latencies decreased with increasing stimulus frequency and CAP amplitudes were correlated with known variations in afferent fibre numbers from the different papillar regions. This suggests a local origin of the CAP along the tonotopic gradient within the basilar papilla. The audiograms derived from CAP and CM threshold responses both showed a broad frequency region of optimal sensitivity, very similar to behavioural and single-unit data, but shifted upward in absolute sensitivity. CAP thresholds rose above 8 kHz, while CM responses showed unchanged sensitivity up to 10 kHz