Mammalian hearing sensitivity and frequency selectivity depend on a mechanical amplification process mediated by outer hair cells (OHCs). OHCs are situated within the organ of Corti atop the basilar membrane (BM), which supports sound-evoked traveling waves. It is well established that OHCs generate force to selectively amplify BM traveling waves where they peak, and that amplification accumulates from one location to the next over this narrow cochlear region. However, recent measurements demonstrate that traveling waves along the apical surface of the organ of Corti, the reticular lamina (RL), are amplified over a much broader region. Whether OHC forces accumulate along the length of the RL traveling wave to provide a form of "global" cochlear amplification is unclear. Here we examined the spatial accumulation of RL amplification. In mice of either sex, we used tones to suppress amplification from different cochlear regions and examined the effect on RL vibrations near and far from the traveling-wave peak. We found that although OHC forces amplify the entire RL traveling wave, amplification only accumulates near the peak, over the same region where BM motion is amplified. This contradicts the notion that RL motion is involved in a global amplification mechanism and reveals that the mechanical properties of the BM and organ of Corti tune how OHC forces accumulate spatially. Restricting the spatial buildup of amplification enhances frequency selectivity by sharpening the peaks of cochlear traveling waves and constrains the number of OHCs responsible for mechanical sensitivity at each location.

Significance The remarkable high-frequency sensitivity of mammalian hearing depends on the amplification of sound-evoked cochlear vibrations by outer hair cells. One way that outer hair cells are proposed to generate amplifying forces is through voltage-driven changes in cell length. However, it remains unclear whether this electromotility can work fast enough in vivo to provide amplification at the necessary frequencies. Here, we show that sound elicits motions within the living mouse cochlea that are fully consistent with electromotility. These motions are large relative to the motion of the underlying cochlear partition, including at high frequencies. The data therefore suggest that electromotility can indeed provide high-speed amplification in vivo.

Neuroplastin (Nptn) is a member of the Ig superfamily and is expressed in two isoforms, Np55 and Np65. Np65 regulates synaptic transmission but the function of Np55 is unknown. In an N-ethyl-N-nitrosaurea mutagenesis screen, we have now generated a mouse line with an Nptn mutation that causes deafness. We show that Np55 is expressed in stereocilia of outer hair cells (OHCs) but not inner hair cells and affects interactions of stereocilia with the tectorial membrane. In vivo vibrometry demonstrates that cochlear amplification is absent in Nptn mutant mice, which is consistent with the failure of OHC stereocilia to maintain stable interactions with the tectorial membrane. Hair bundles show morphological defects as the mutant mice age and while mechanotransduction currents can be evoked in early postnatal hair cells, cochlea microphonics recordings indicate that mechanontransduction is affected as the mutant mice age. We thus conclude that differential splicing leads to functional diversification of Nptn, where Np55 is essential for OHC function, while Np65 is implicated in the regulation of synaptic function.

The purpose was to determine the effect of hearing loss on the ability to separate competing talkers using talker differences in fundamental frequency (F0) and apparent vocal-tract length (VTL). Performance of 13 adults with hearing loss and 6 adults with normal hearing was measured using the Coordinate Response Measure. For listeners with hearing loss, the speech was amplified and filtered according to the NAL-RP hearing aid prescription. Target-to-competition ratios varied from 0 to 9 dB. The target sentence was randomly assigned to the higher or lower values of F0 or VTL on each trial. Performance improved for F0 differences up to 9 and 6 semitones for people with normal hearing and hearing loss, respectively, but only when the target talker had the higher F0. Recognition for the lower F0 target improved when trial-to-trial uncertainty was removed (9-semitone condition). Scores improved with increasing differences in VTL for the normal-hearing group. On average, hearing-impaired listeners did not benefit from VTL cues, but substantial inter-subject variability was observed. The amount of benefit from VTL cues was related to the average hearing loss in the 1-3-kHz region when the target talker had the shorter VTL.

The stereociliary bundles of cochlear hair cells convert mechanical vibrations into the electrical signals required for auditory sensation. While the stiffness of the bundles strongly influences mechanotransduction, its influence on the vibratory response of the cochlear partition is unclear. To assess this, we measured cochlear vibrations in mutant mice with reduced bundle stiffness or with a tectorial membrane (TM) that is detached from the sensory epithelium. We found that reducing bundle stiffness decreased the high-frequency extent and sharpened the tuning of vibratory responses obtained postmortem. Detaching the TM further reduced the high-frequency extent of the vibrations but also lowered the partition's resonant frequency. Together, these results demonstrate that the bundle's stiffness and attachment to the TM contribute to passive longitudinal coupling in the cochlea. We conclude that the stereociliary bundles and TM interact to facilitate passive-wave propagation to more apical locations, possibly enhancing active-wave amplification in vivo.