Outer Hair Cells and Electromotility

Ashmore, Jonathan

doi:10.1101/cshperspect.a033522

Cited by 37 publications

(24 citation statements)

References 53 publications

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“…Conversely, SLC7A14, OTOF, and SLC17A8 are prominent inner hair cell markers and OCM is an outer hair cell marker in mammals, yet these genes are expressed in all chicken hair cells (Figure S5B). Prestin, encoded by SLC26A5, is a prominent outer hair cell gene (Ashmore, 2019). Although SLC26A5 mRNA is found sporadically in chicken basilar papilla hair cells, we did not find the gene to be differentially enriched in short hair cells (Figure S5B).…”

Section: Discussionmentioning

confidence: 66%

Cell-type identity of the avian cochlea

et al. 2021

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Section: Discussionmentioning

confidence: 66%

Cell-type identity of the avian cochlea

et al. 2021

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“…The analysis is agnostic to the specific molecules responsible for piezoelectricity but places constraints on what is thermodynamically feasible. It is known that OHC electromotility requires expression of the transmembrane protein prestin , a member of the SLC26 family of anion transporters ( 3 , 31 , 32 ). There is strong evidence that Cl − is essential and is electrostatically bound in the central core region of the protein ( 33 – 35 ).…”

Section: Discussionmentioning

confidence: 99%

The cochlear outer hair cell speed paradox

Rabbitt

2020

Proc. Natl. Acad. Sci. U.S.A.

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Cochlear outer hair cells (OHCs) are among the fastest known biological motors and are essential for high-frequency hearing in mammals. It is commonly hypothesized that OHCs amplify vibrations in the cochlea through cycle-by-cycle changes in length, but recent data suggest OHCs are low-pass filtered and unable to follow high-frequency signals. The fact that OHCs are required for high-frequency hearing but appear to be throttled by slow electromotility is the “OHC speed paradox.” The present report resolves this paradox and reveals origins of ultrafast OHC function and power output in the context of the cochlear load. Results demonstrate that the speed of electromotility reflects how fast the cell can extend against the load, and does not reflect the intrinsic speed of the motor element itself or the nearly instantaneous speed at which the coulomb force is transmitted. OHC power output at auditory frequencies is revealed by emergence of an imaginary nonlinear capacitance reflecting the phase of electrical charge displacement required for the motor to overcome the viscous cochlear load.

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“…In mammals, normal hearing depends on the ability of the cochlea to amplify acoustic stimuli (Ashmore, 2019). This amplification is provided by the OHCs, which generate voltage‐dependent axial forces driving electromotility (Brownell et al .…”

Section: Introductionmentioning

confidence: 99%

Age‐related changes in the biophysical and morphological characteristics of mouse cochlear outer hair cells

Jeng

Johnson

Carlton

et al. 2020

The Journal of Physiology

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Key points Age‐related hearing loss (ARHL) is a very heterogeneous disease, resulting from cellular senescence, genetic predisposition and environmental factors (e.g. noise exposure). Currently, we know very little about age‐related changes occurring in the auditory sensory cells, including those associated with the outer hair cells (OHCs). Using different mouse strains, we show that OHCs undergo several morphological and biophysical changes in the ageing cochlea. Ageing OHCs also exhibited the progressive loss of afferent and efferent synapses. We also provide evidence that the size of the mechanoelectrical transducer current is reduced in ageing OHCs, highlighting its possible contribution in cochlear ageing. Abstract Outer hair cells (OHCs) are electromotile sensory receptors that provide sound amplification within the mammalian cochlea. Although OHCs appear susceptible to ageing, the progression of the pathophysiological changes in these cells is still poorly understood. By using mouse strains with a different progression of hearing loss (C57BL/6J, C57BL/6NTac, C57BL/6NTacCdh23+, C3H/HeJ), we have identified morphological, physiological and molecular changes in ageing OHCs (9–12 kHz cochlear region). We show that by 6 months of age, OHCs from all strains underwent a reduction in surface area, which was not a sign of degeneration. Although the ageing OHCs retained a normal basolateral membrane protein profile, they showed a reduction in the size of the K+ current and non‐linear capacitance, a readout of prestin‐dependent electromotility. Despite these changes, OHCs have a normal Vm and retain the ability to amplify sound, as distortion product otoacoustic emission thresholds were not affected in aged, good‐hearing mice (C3H/HeJ, C57BL/6NTacCdh23+). The loss of afferent synapses was present in all strains at 15 months. The number of efferent synapses per OHCs, defined as postsynaptic SK2 puncta, was reduced in aged OHCs of all strains apart from C3H mice. Several of the identified changes occurred in aged OHCs from all mouse strains, thus representing a general trait in the pathophysiological progression of age‐related hearing loss, possibly aimed at preserving functionality. We have also shown that the mechanoelectrical transduction (MET) current from OHCs of mice harbouring the Cdh23ahl allele is reduced with age, highlighting the possibility that changes in the MET apparatus could play a role in cochlear ageing.

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Outer Hair Cells and Electromotility

Cited by 37 publications

References 53 publications

Cell-type identity of the avian cochlea

Cell-type identity of the avian cochlea

The cochlear outer hair cell speed paradox

Age‐related changes in the biophysical and morphological characteristics of mouse cochlear outer hair cells

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