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According to the dominant view, the mammalian cochlea spatially amplifies signals by actively pumping energy into the traveling wave. That is, signals are amplified as they propagate through a region where the medium's resistance is effectively negative. While signal amplification has been extensively studied in active cochlear models, the same cannot be said for amplification of internal noise. According to transmission-line theory, signals are amplified more than internal noise in regions where the net resistance is negative. Here we generalize this finding by showing that a distributed system composed of cascaded "noisy" amplifiers boosts signals more rapidly than the internal noise; the larger the amplifier gain, the larger the signal-to-noise ratio (SNR) of the amplified signal. We further show that this mechanism operates in existing active cochlear models: the cochlear amplifier increases the SNR of cochlear responses, and thus enhances cochlear sensitivity. When considering also that the cochlear amplifier narrows the bandwidth of the "cochlear filters", activation of the cochlear amplifiers dramatically increases the SNR (by about one order of magnitude in our simulations) from the tail to the peak of the traveling wave. We further demonstrate that the tapered ear-horn-like cochlear geometry significantly improves the SNR of basilar-membrane responses. [ABSTRACT FROM AUTHOR]

Two hydrodynamic effects are introduced in the standard transmission-line formalism, the focusing of the pressure and fluid velocity fields near the basilar membrane and the viscous damping at the fluid-basilar membrane interface, which significantly affect the cochlear response in the short-wave region. In this region, in which the wavelength is shorter than the cochlear duct height, only a layer of fluid of order of the wavelength is effectively involved in the traveling wave. This has been interpreted [8] as a reduced fluid contribution to the system inertia in the peak region, which is a viewpoint common to the 3-D FEM solutions. In this paper we propose an alternative approach, from a slightly different physical viewpoint. Invoking the fluid flux conservation along the traveling wave propagation direction, we can derive a rigorous propagation equation for the pressure integrated along the vertical axis. Consequently, the relation between the average pressure and the local pressure [4] at the fluid-BM interface can be written. The local pressure is amplified by a factor dependent on the local wavenumber with respect to the average pressure, a phenomenon we refer to as "fluid focusing", which plays a relevant role in the BM total amplification gain. This interpretation of the hydrodynamic boost to the pressure provides a physical justification to the strategy [10] of fitting the BM admittance with a polynomial containing both a conjugated pole and a zero. In the short-wave region, the sharp gradients of the velocity field yield a second important effect, a damping force on the BM motion, proportional to the local wavenumber, which stabilizes active models and shifts the peak of the response towards the base, with respect to the resonant place. This way, the peaked BM response is not that of a proper resonance, corresponding to a sharp maximum of the admittance, but rather a focusing-driven growth toward the resonant place, which is "aborted" before reaching it by the sharply increasing viscous losses. The large values of the wavenumber that ensure strong focusing are ultimately fueled, against viscosity, by the nonlinear OHC mechanism, hence the otherwise puzzling observation of a wide nonlinear gain dynamics with almost level-independent admittance. [ABSTRACT FROM AUTHOR]

The inner hair cells of the mammalian cochlea transform the vibrations of their stereocilia into releases of neurotransmitter at the ribbon synapses, thereby controlling the activity of the afferent auditory fibers. The mechanical-to-neural transduction is a highly nonlinear process and it introduces differences between the frequency-tuning of the stereocilia and that of the afferent fibers. Using a computational model of the inner hair cell that is based on in vitro data, we estimated that smaller vibrations of the stereocilia are necessary to drive the afferent fibers above threshold at low (≤0.5 kHz) than at high (≥4 kHz) driving frequencies. In the base of the cochlea, the transduction process affects the low-frequency tails of neural tuning curves. In particular, it introduces differences between the frequency-tuning of the stereocilia and that of the auditory fibers resembling those between basilar membrane velocity and auditory fibers tuning curves in the chinchilla base. For units with a characteristic frequency between 1 and 4 kHz, the transduction process yields shallower neural than stereocilia tuning curves as the characteristic frequency decreases. This study proposes that transduction contributes to the progressive broadening of neural tuning curves from the base to the apex. [ABSTRACT FROM AUTHOR]

The response of an inner hair cell (IHC) to a sound stimulus varies in terms of phase and harmonic content depending nonlinearly on the stimulus level. This dependency can be explained by the two factor cancellation hypothesis: two excitatory components of the opposite sign, C1 and C2, regulate the IHC receptor potential. However, it is yet unknown whether C1 and C2 represent the contribution of different stereocilia rows to the transduction of a single IHC, or whether they represent different mechanical contributions to the displacement of a single stereocilia bundle. There are also diverse theories about the physical origin of the two components. This work presents a computational model of IHCs functionality having clear physical origins for C1 and C2. In the present model C1 represents the transduction component associated with the coupling between the stereocilia and the basilar membrane (BM), while C2 represents the transduction component associated with the coupling between the stereocilia and the outer hair cells (OHCs). C1 and C2 are derived from the nonlinear cochlear model by Verhulst et al. (2012). In particular, C1 is derived from the BM velocity vector and C2 is derived from the term representing the action of the organ of Corti (OC) on BM motion. The present model is capable to simulate the dynamic response of IHCs and to emulate the dependency of the phase and harmonic content of IHCs response, being in good agreement with animal data. Furthermore, this work introduces a simple physical interpretation of C2 to phenomenological models of two-factor cancellation. [ABSTRACT FROM AUTHOR]

The response of an inner hair cell (IHC) to a sound stimulus varies in terms of phase and harmonic content depending nonlinearly on the stimulus level. This dependency can be explained by the two factor cancellation hypothesis: two excitatory components of the opposite sign, C1 and C2, regulate the IHC receptor potential. However, it is yet unknown whether C1 and C2 represent the contribution of different stereocilia rows to the transduction of a single IHC, or whether they represent different mechanical contributions to the displacement of a single stereocilia bundle. There are also diverse theories about the physical origin of the two components. This work presents a computational model of IHCs functionality having clear physical origins for C1 and C2. In the present model C1 represents the transduction component associated with the coupling between the stereocilia and the basilar membrane (BM), while C2 represents the transduction component associated with the coupling between the stereocilia and the outer hair cells (OHCs). C1 and C2 are derived from the nonlinear cochlear model by Verhulst et al. (2012). In particular, C1 is derived from the BM velocity vector and C2 is derived from the term representing the action of the organ of Corti (OC) on BM motion. The present model is capable to simulate the dynamic response of IHCs and to emulate the dependency of the phase and harmonic content of IHCs response, being in good agreement with animal data. Furthermore, this work introduces a simple physical interpretation of C2 to phenomenological models of two-factor cancellation. [ABSTRACT FROM AUTHOR]