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      Modelling Cochlear Mechanics

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          Abstract

          The cochlea plays a crucial role in mammal hearing. The basic function of the cochlea is to map sounds of different frequencies onto corresponding characteristic positions on the basilar membrane (BM). Sounds enter the fluid-filled cochlea and cause deflection of the BM due to pressure differences between the cochlear fluid chambers. These deflections travel along the cochlea, increasing in amplitude, until a frequency-dependent characteristic position and then decay away rapidly. The hair cells can detect these deflections and encode them as neural signals. Modelling the mechanics of the cochlea is of help in interpreting experimental observations and also can provide predictions of the results of experiments that cannot currently be performed due to technical limitations. This paper focuses on reviewing the numerical modelling of the mechanical and electrical processes in the cochlea, which include fluid coupling, micromechanics, the cochlear amplifier, nonlinearity, and electrical coupling.

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          A cochlear frequency-position function for several species--29 years later.

          Accurate cochlear frequency-position functions based on physiological data would facilitate the interpretation of physiological and psychoacoustic data within and across species. Such functions might aid in developing cochlear models, and cochlear coordinates could provide potentially useful spectral transforms of speech and other acoustic signals. In 1961, an almost-exponential function was developed (Greenwood, 1961b, 1974) by integrating an exponential function fitted to a subset of frequency resolution-integration estimates (critical bandwidths). The resulting frequency-position function was found to fit cochlear observations on human cadaver ears quite well and, with changes of constants, those on elephant, cow, guinea pig, rat, mouse, and chicken (Békésy, 1960), as well as in vivo (behavioral-anatomical) data on cats (Schucknecht, 1953). Since 1961, new mechanical and other physiological data have appeared on the human, cat, guinea pig, chinchilla, monkey, and gerbil. It is shown here that the newer extended data on human cadaver ears and from living animal preparations are quite well fit by the same basic function. The function essentially requires only empirical adjustment of a single parameter to set an upper frequency limit, while a "slope" parameter can be left constant if cochlear partition length is normalized to 1 or scaled if distance is specified in physical units. Constancy of slope and form in dead and living ears and across species increases the probability that the function fitting human cadaver data may apply as well to the living human ear. This prospect increases the function's value in plotting auditory data and in modeling concerned with speech and other bioacoustic signals, since it fits the available physiological data well and, consequently (if those data are correct), remains independent of, and an appropriate means to examine, psychoacoustic data and assumptions.
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            Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier.

            Hearing sensitivity in mammals is enhanced by more than 40 dB (that is, 100-fold) by mechanical amplification thought to be generated by one class of cochlear sensory cells, the outer hair cells. In addition to the mechano-electrical transduction required for auditory sensation, mammalian outer hair cells also perform electromechanical transduction, whereby transmembrane voltage drives cellular length changes at audio frequencies in vitro. This electromotility is thought to arise through voltage-gated conformational changes in a membrane protein, and prestin has been proposed as this molecular motor. Here we show that targeted deletion of prestin in mice results in loss of outer hair cell electromotility in vitro and a 40-60 dB loss of cochlear sensitivity in vivo, without disruption of mechano-electrical transduction in outer hair cells. In heterozygotes, electromotility is halved and there is a twofold (about 6 dB) increase in cochlear thresholds. These results suggest that prestin is indeed the motor protein, that there is a simple and direct coupling between electromotility and cochlear amplification, and that there is no need to invoke additional active processes to explain cochlear sensitivity in the mammalian ear.
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              Cochlear outer hair cell motility.

              Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential. The forces depend on the presence of a motor protein in the lateral membrane of the cells. This protein, known as prestin, is a member of a transporter superfamily SLC26. The functional and structural properties of prestin are described in this review. Whether outer hair cell motility might account for sound amplification at all frequencies is also a critical question and is reviewed here.
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                Author and article information

                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi Publishing Corporation
                2314-6133
                2314-6141
                2014
                23 July 2014
                : 2014
                : 150637
                Affiliations
                1Institute of Sound and Vibration Research, University of Southampton, Southampton SO17 1BJ, UK
                2School of Engineering and Computer Science, Victoria University of Wellington, P.O. Box 600, Wellington 6140, New Zealand
                Author notes

                Academic Editor: Frank Böhnke

                Author information
                http://orcid.org/0000-0002-9240-3020
                http://orcid.org/0000-0003-2310-6257
                Article
                10.1155/2014/150637
                4130145
                25136555
                d8a33c32-6009-4faf-80b8-b31b69c6a770
                Copyright © 2014 Guangjian Ni et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 January 2014
                : 2 June 2014
                Categories
                Review Article

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