Nonlinearity of Mechanoelectrical Transduction of Outer Hair Cells as the Source of Nonlinear Basilar-Membrane Motion and Loudness Recruitment

1996 ◽  
Vol 1 (1) ◽  
pp. 3-11 ◽  
Author(s):  
Serena Preyer ◽  
Anthony W. Gummer
2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Victoria A. Lukashkina ◽  
Snezana Levic ◽  
Andrei N. Lukashkin ◽  
Nicola Strenzke ◽  
Ian J. Russell

Abstract Accelerated age-related hearing loss disrupts high-frequency hearing in inbred CD-1 mice. The p.Ala88Val (A88V) mutation in the gene coding for the gap-junction protein connexin30 (Cx30) protects the cochlear basal turn of adult CD-1Cx30 A88V/A88V mice from degeneration and rescues hearing. Here we report that the passive compliance of the cochlear partition and active frequency tuning of the basilar membrane are enhanced in the cochleae of CD-1Cx30 A88V/A88V compared to CBA/J mice with sensitive high-frequency hearing, suggesting that gap junctions contribute to passive cochlear mechanics and energy distribution in the active cochlea. Surprisingly, the endocochlear potential that drives mechanoelectrical transduction currents in outer hair cells and hence cochlear amplification is greatly reduced in CD-1Cx30 A88V/A88V mice. Yet, the saturating amplitudes of cochlear microphonic potentials in CD-1Cx30 A88V/A88V and CBA/J mice are comparable. Although not conclusive, these results are compatible with the proposal that transmembrane potentials, determined mainly by extracellular potentials, drive somatic electromotility of outer hair cells.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Haim Sohmer

The three modes of auditory stimulation (air, bone and soft tissue conduction) at threshold intensities are thought to share a common excitation mechanism: the stimuli induce passive displacements of the basilar membrane propagating from the base to the apex (slow mechanical traveling wave), which activate the outer hair cells, producing active displacements, which sum with the passive displacements. However, theoretical analyses and modeling of cochlear mechanics provide indications that the slow mechanical basilar membrane traveling wave may not be able to excite the cochlea at threshold intensities with the frequency discrimination observed. These analyses are complemented by several independent lines of research results supporting the notion that cochlear excitation at threshold may not involve a passive traveling wave, and the fast cochlear fluid pressures may directly activate the outer hair cells: opening of the sealed inner ear in patients undergoing cochlear implantation is not accompanied by threshold elevations to low frequency stimulation which would be expected to result from opening the cochlea, reducing cochlear impedance, altering hydrodynamics. The magnitude of the passive displacements at threshold is negligible. Isolated outer hair cells in fluid display tuned mechanical motility to fluid pressures which likely act on stretch sensitive ion channels in the walls of the cells. Vibrations delivered to soft tissue body sites elicit hearing. Thus, based on theoretical and experimental evidence, the common mechanism eliciting hearing during threshold stimulation by air, bone and soft tissue conduction may involve the fast-cochlear fluid pressures which directly activate the outer hair cells.


2019 ◽  
Vol 116 (41) ◽  
pp. 20743-20749 ◽  
Author(s):  
Maryline Beurg ◽  
Amanda Barlow ◽  
David N. Furness ◽  
Robert Fettiplace

Mechanoelectrical transducer (MET) currents were recorded from cochlear hair cells in mice with mutations of transmembrane channel-like protein TMC1 to study the effects on MET channel properties. We characterized a Tmc1 mouse with a single-amino-acid mutation (D569N), homologous to a dominant human deafness mutation. Measurements were made in both Tmc2 wild-type and Tmc2 knockout mice. By 30 d, Tmc1 pD569N heterozygote mice were profoundly deaf, and there was substantial loss of outer hair cells (OHCs). MET current in OHCs of Tmc1 pD569N mutants developed over the first neonatal week to attain a maximum amplitude one-third the size of that in Tmc1 wild-type mice, similar at apex and base, and lacking the tonotopic size gradient seen in wild type. The MET-channel Ca2+ permeability was reduced 3-fold in Tmc1 pD569N homozygotes, intermediate deficits being seen in heterozygotes. Reduced Ca2+ permeability resembled that of the Tmc1 pM412K Beethoven mutant, a previously studied semidominant mouse mutation. The MET channel unitary conductance, assayed by single-channel recordings and by measurements of current noise, was unaffected in mutant apical OHCs. We show that, in contrast to the Tmc1 M412K mutant, there was reduced expression of the TMC1 D569N channel at the transduction site assessed by immunolabeling, despite the persistence of tip links. The reduction in MET channel Ca2+ permeability seen in both mutants may be the proximate cause of hair-cell apoptosis, but changes in bundle shape and protein expression in Tmc1 D569N suggest another role for TMC1 apart from forming the channel.


Nature ◽  
2004 ◽  
Vol 429 (6993) ◽  
pp. 766-770 ◽  
Author(s):  
David Z. Z. He ◽  
Shuping Jia ◽  
Peter Dallos

2020 ◽  
Author(s):  
C. Elliott Strimbu ◽  
Yi Wang ◽  
Elizabeth S. Olson

ABSTRACTThe mammalian hearing organ, the cochlea, contains an active amplifier to boost the vibrational response to low level sounds. Hallmarks of this active process are sharp location-dependent frequency tuning and compressive nonlinearity over a wide stimulus range. The amplifier relies on outer hair cell (OHC) generated forces driven in part by the endocochlear potential (EP), the ~ +80 mV potential maintained in scala media, generated by the stria vascularis. We transiently eliminated the EP in vivo by an intravenous injection of furosemide and measured the vibrations of different layers in the cochlea’s organ of Corti using optical coherence tomography. Distortion product otoacoustic emissions (DPOAE) were monitored at the same times. Following the injection, the vibrations of the basilar membrane lost the best frequency (BF) peak and showed broad tuning similar to a passive cochlea. The intra-organ of Corti vibrations measured in the region of the OHCs lost their BF peak and showed low-pass responses, but retained nonlinearity, indicating that OHC electromotility was still operational. Thus, while electromotility is presumably necessary for amplification, its presence is not sufficient for amplification. The BF peak recovered nearly fully within 2 hours, along with a non-monotonic DPOAE recovery that suggests that physical shifts in operating condition are a final step in the recovery process.SIGNIFICANCEThe endocochlear potential, the +80 mV potential difference across the fluid filled compartments of the cochlea, is essential for normal mechanoelectrical transduction, which leads to receptor potentials in the sensory hair cells when they vibrate in response to sound. Intracochlear vibrations are boosted tremendously by an active nonlinear feedback process that endows the cochlea with its healthy sensitivity and frequency resolution. When the endocochlear potential was reduced by an injection of furosemide, the basilar membrane vibrations resembled those of a passive cochlea, with broad tuning and linear scaling. The vibrations in the region of the outer hair cells also lost the tuned peak, but retained nonlinearity at frequencies below the peak, and these sub-BF responses recovered fairly rapidly. Vibration responses at the peak recovered nearly fully over 2 hours. The staged vibration recovery and a similarly staged DPOAE recovery suggests that physical shifts in operating condition are a final step in the process of cochlear recovery.


Author(s):  
Amitava Biswas

The human ear is often regarded as a paragon of mechanical engineering. To understand how the hearing system works, scientists have proposed detailed models of its specific aspects—the transfer of acoustic energy from the atmosphere to the tympanic membrane via the external ear; the coupling of the tympanic membrane to the oval window of the cochlea via ossicles; the resultant fluidic oscillations in the cochlear ducts; the formation of traveling waves in the basilar membrane of the cochlea; the mechanical stimulation of inner hair cells by the basilar membrane; and the consequential transduction of nerve impulses. Scientists have also proposed models to explain the phenomenon of enhancement of the traveling waves in the basilar membrane by synchronized co-contraction in the length of outer hair cells (OHCs). Although it is unrealistic that any OHC would contract in length without expanding in diameter, the models proposed by other analysts have so far incorporated the longitudinal contraction of OHCs only, suggesting that the impact of any diametric expansion of OHCs would be relatively trival. Here we show that the basilar membrane would behave like a Beam-Column system, which may be significantly influenced by the diametric expansion of OHCs.


1999 ◽  
Vol 82 (5) ◽  
pp. 2798-2807 ◽  
Author(s):  
Xintian Hu ◽  
Burt N. Evans ◽  
Peter Dallos

The basilar membrane in the mammalian cochlea vibrates when the cochlea receives a sound stimulus. This mechanical vibration is transduced into hair cell receptor potentials and thereafter encoded by action potentials in the auditory nerve. Knowledge of the mechanical transformation that converts basilar membrane vibration into hair cell stimulation has been limited, until recently, to hypothetical geometric models. Experimental observations are largely lacking to prove or disprove the validity of these models. We have developed a hemicochlea preparation to visualize the kinematics of the cochlear micromechanism. Direct mechanical drive of 1–2 Hz sinusoidal command was applied to the basilar membrane. Vibration patterns of the basilar membrane, inner and outer hair cells, supporting cells, and tectorial membrane have been recorded concurrently by means of a video optical flow technique. Basilar membrane vibration was driven in a direction transversal to its plane. However, the direction of the resulting vibration was found to be essentially radial at the level of the reticular lamina and cuticular plates of inner and outer hair cells. The tectorial membrane vibration was mainly transversal. The transmission ratio between cilia displacement of inner and outer hair cells and basilar membrane vibration is in the range of 0.7–1.1. These observations support, in part, the classical geometric models at low frequencies. However, there appears to be less tectorial membrane motion than predicted, and it is largely in the transversal direction.


1992 ◽  
Vol 336 (1278) ◽  
pp. 317-324 ◽  

Receptor potentials recorded from outer hair cells (ohc ) and inner hair cells (ihc) in the basal highfrequency turn were com pared. The dc component of the ihc receptor potential is maximized to ensure that ihcs can signal a voltage response to high-frequency tones. The ohc dc component is minimized so that ohcs transduce in the most sensitive region of their operating range. The phase and magnitude of ohc receptor potentials were recorded as an indicator of the magnitude and phase of the energy which is fed back to the basilar membrane to provide the basis for the sharp tuning and fine sensitivity of the cochlea to tones. IHC receptor potentials were recorded to assess the net effect of the feedback on the mechanics of the cochlea. It was concluded that ohcs generate feedback which enhances the ihc responses only at the best frequency. At frequencies below cf, ihc dc responses are elicited only when the ohc ac responses begin to saturate.


2002 ◽  
Vol 164 (1-2) ◽  
pp. 190-205 ◽  
Author(s):  
Claudia C. Schulte ◽  
Jens Meyer ◽  
David N. Furness ◽  
Carole M. Hackney ◽  
Thomas R. Kleyman ◽  
...  

2018 ◽  
Vol 10 (4) ◽  
pp. 48
Author(s):  
Valeri Goussev

The article is devoted to the specific consideration of the cochlear transduction for the low level sound intensities, which correspond to the regions near the perception threshold. The basic cochlea mechanics is extended by the new concept of the molecular filters, which allows discussing the transduction mechanism on the molecular level in the space-time domain. The molecular filters are supposed to be built on the set of the stereocilia of every inner hair cell. It is hypothesized that the molecular filters are the sensors in the feedback loop, which includes also outer hair cells along with the tectorial membrane and uses the zero compensation method to evaluate the traveling wave shape on the basilar membrane. Besides the compensation, the feedback loop, being spatially distributed along the cochlea, takes control over the tectorial membrane strain field generated by the outer hair cells, and implements it as the mechanism for the automatic gain control in the sound transduction.


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