scholarly journals Prestin-Driven Cochlear Amplification Is Not Limited by the Outer Hair Cell Membrane Time Constant

Neuron ◽  
2011 ◽  
Vol 70 (6) ◽  
pp. 1143-1154 ◽  
Author(s):  
Stuart L. Johnson ◽  
Maryline Beurg ◽  
Walter Marcotti ◽  
Robert Fettiplace
Keyword(s):  
Cell Membrane ◽  
Hair Cell ◽  
Time Constant ◽  
Outer Hair Cell ◽  
Membrane Time Constant ◽  
Cochlear Amplification

scholarly journals Outer hair cell electromotility is low-pass filtered relative to the molecular conformational changes that produce nonlinear capacitance

2019 ◽  
Vol 151 (12) ◽  
pp. 1369-1385 ◽  
Author(s):  
Joseph Santos-Sacchi ◽  
Kuni H. Iwasa ◽  
Winston Tan
Keyword(s):  
Guinea Pig ◽  
Hair Cell ◽  
Frequency Response ◽  
Time Constant ◽  
Outer Hair Cell ◽  
Resting Potential ◽  
Nonlinear Capacitance ◽  
Cochlear Amplification ◽  
Low Pass ◽  
Length Changes

The outer hair cell (OHC) of the organ of Corti underlies a process that enhances hearing, termed cochlear amplification. The cell possesses a unique voltage-sensing protein, prestin, that changes conformation to cause cell length changes, a process termed electromotility (eM). The prestin voltage sensor generates a capacitance that is both voltage- and frequency-dependent, peaking at a characteristic membrane voltage (Vh), which can be greater than the linear capacitance of the OHC. Accordingly, the OHC membrane time constant depends upon resting potential and the frequency of AC stimulation. The confounding influence of this multifarious time constant on eM frequency response has never been addressed. After correcting for this influence on the whole-cell voltage clamp time constant, we find that both guinea pig and mouse OHC eM is low pass, substantially attenuating in magnitude within the frequency bandwidth of human speech. The frequency response is slowest at Vh, with a cut-off, approximated by single Lorentzian fits within that bandwidth, near 1.5 kHz for the guinea pig OHC and near 4.3 kHz for the mouse OHC, each increasing in a U-shaped manner as holding voltage deviates from Vh. Nonlinear capacitance (NLC) measurements follow this pattern, with cut-offs about double that for eM. Macro-patch experiments on OHC lateral membranes, where voltage delivery has high fidelity, confirms low pass roll-off for NLC. The U-shaped voltage dependence of the eM roll-off frequency is consistent with prestin’s voltage-dependent transition rates. Modeling indicates that the disparity in frequency cut-offs between eM and NLC may be attributed to viscoelastic coupling between prestin’s molecular conformations and nanoscale movements of the cell, possibly via the cytoskeleton, indicating that eM is limited by the OHC’s internal environment, as well as the external environment. Our data suggest that the influence of OHC eM on cochlear amplification at higher frequencies needs reassessment.

Modeling the Mechanics of Tethers Pulled From the Cochlear Outer Hair Cell Membrane

2008 ◽  
Vol 130 (3) ◽  
Author(s):  
Kristopher R. Schumacher ◽  
Aleksander S. Popel ◽  
Bahman Anvari ◽  
William E. Brownell ◽  
Alexander A. Spector
Keyword(s):  
Cell Membrane ◽  
Hair Cell ◽  
Outer Hair Cell ◽  
Lateral Wall ◽  
Outer Hair Cells ◽  
The Body ◽  
Computational Method ◽  
Membrane Properties ◽  
Bending Modulus ◽  
Sound Amplification

Cell membrane tethers are formed naturally (e.g., in leukocyte rolling) and experimentally to probe membrane properties. In cochlear outer hair cells, the plasma membrane is part of the trilayer lateral wall, where the membrane is attached to the cytoskeleton by a system of radial pillars. The mechanics of these cells is important to the sound amplification and frequency selectivity of the ear. We present a modeling study to simulate the membrane deflection, bending, and interaction with the cytoskeleton in the outer hair cell tether pulling experiment. In our analysis, three regions of the membrane are considered: the body of a cylindrical tether, the area where the membrane is attached and interacts with the cytoskeleton, and the transition region between the two. By using a computational method, we found the shape of the membrane in all three regions over a range of tether lengths and forces observed in experiments. We also analyze the effects of biophysical properties of the membrane, including the bending modulus and the forces of the membrane adhesion to the cytoskeleton. The model’s results provide a better understanding of the mechanics of tethers pulled from cell membranes.

Elastic moduli of the piezoelectric cochlear outer hair cell membrane

2003 ◽  
Vol 43 (3) ◽  
pp. 355-360 ◽  
Author(s):  
A. A. Spector ◽  
R. P. Jean
Keyword(s):  
Cell Membrane ◽  
Hair Cell ◽  
Elastic Moduli ◽  
Outer Hair Cell

scholarly journals Electrical property in outer hair cell membrane of guinea-pig cochlea

1992 ◽  
Vol 58 ◽  
pp. 269
Author(s):  
Seiji Kakehata ◽  
Takashi Nakagawa ◽  
Norio Akaike
Keyword(s):  
Electrical Property ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Hair Cell ◽  
Outer Hair Cell ◽  
Guinea Pig Cochlea

An outer hair cell-powered global hydromechanical mechanism for cochlear amplification

2021 ◽  
pp. 108407
Author(s):  
Wenxuan He ◽  
George Burwood ◽  
Anders Fridberger ◽  
Alfred L. Nuttall ◽  
Tianying Ren
Keyword(s):  
Hair Cell ◽  
Outer Hair Cell ◽  
Cochlear Amplification

Theory of electrically driven shape changes of cochlear outer hair cells

1993 ◽  
Vol 70 (1) ◽  
pp. 299-323 ◽  
Author(s):  
P. Dallos ◽  
R. Hallworth ◽  
B. N. Evans
Keyword(s):  
Cell Membrane ◽  
Hair Cell ◽  
Outer Hair Cell ◽  
Linear Motor ◽  
Outer Hair Cells ◽  
Pressure Effects ◽  
Model Parameters ◽  
Minor Importance ◽  
Length Changes ◽  
Shape Changes

1. A theory of cochlear outer hair cell electromotility is developed and specifically applied to somatic shape changes elicited in a microchamber. The microchamber permits the arbitrary electrical and mechanical partitioning of the outer hair cell along its length. This means that the two partitioned segments are stimulated with different input voltages and undergo different shape changes. Consequently, by imposing more constraints than other methods, experiments in the microchamber are particularly suitable for testing different theories of outer hair cell motility. 2. The present model is based on simple hypotheses. They include a distributed motor associated with the cell membrane or cortex and the assumption that the displacement generated by the motor is related to the transmembrane voltage across the associated membrane element. It is expected that the force generated by the motor is counterbalanced by an elastic restoring force indigenous to the cell membrane and cortex, and a tensile force due to intracellular pressure. It is assumed that all changes take place while total cell volume is conserved. The above elements of the theory taken together permit the development of qualitative and quantitative predictions about the expected motile responses of both partitioned segments of the cell. Only a DC treatment is offered here. 3. Both a linear motor and an expanded treatment that incorporates a stochastic molecular motor model are considered. The latter is represented by a two-state Boltzmann process. We show that the linear motor treatment is an appropriate extrapolation of the stochastic motor theory for the case of small voltage driving signals. Comparison of experimental results with model responses permits the estimation of model parameters. Good match of data is obtained if it is assumed that the molecular motors undergo conformational length changes of 0.7-1.0 nm, that they have an effective displacement vector at approximately -20 degrees with the long axis of the cell, and that their linear density is approximately 80/microns. 4. An effort is made to parcel out motile response components that are a direct consequence of the motor action from those that are mediated by cytoplasmic pressure changes brought about by the concerted action of the motors. We show that pressure effects are of minor importance, and thus rule out models that rely on radial constriction/expansion-mediated internal pressure change as the primary cause of longitudinal motility. 5. As a consequence of the interaction between the Boltzmann process and the mechanical characteristics of the cell, the electromotile response is asymmetric.(ABSTRACT TRUNCATED AT 400 WORDS)

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