It is possible for a cochlear model without active negative damping to exhibit a mechanical response peak that is arbitrarily high and arbitrarily wide. Conventional active models rely on external energy inputs to the cochlea to produce the required peak shape. The new model proposed here produces very similar response profiles by assuming that outer hair cell stereocilia stiffness suppresses the mechanical motion in all regions basal of the response peak. Therefore, the model is not active in the usual sense of adding energy to the cochlea. The model suggests a reason for the differing basilar membrane structure in the arcuate and pectinate zones and simulates in vivo and postmortem responses similar to those measured in the real cochlea.
Normal mammalian hearing is refined by amplification of the motion of the cochlear partition. This partition, comprising the organ of Corti sandwiched between the basilar and tectorial membranes, contains the outer hair cells that are thought to drive this amplification process. Force generation by outer hair cells has been studied extensively in vitro and in situ , but, to understand cochlear amplification fully, it is necessary to characterize the role played by each of the components of the cochlear partition in vivo . Observations of cochlear partition motion in vivo are severely restricted by its inaccessibility and sensitivity to surgical trauma, so, for the present study, a computer model has been used to simulate the operation of the cochlea under different experimental conditions. In this model, which uniquely retains much of the three-dimensional complexity of the real cochlea, the motions of the basilar and tectorial membranes are fundamentally different during in situ - and in vivo -like conditions. Furthermore, enhanced outer hair cell force generation in vitro leads paradoxically to a decrease in the gain of the cochlear amplifier during sound stimulation to the model in vivo . These results suggest that it is not possible to extrapolate directly from experimental observations made in vitro and in situ to the normal operation of the intact organ in vivo .
Most types of behaviour, from muscle contraction to conscious thought, are mediated at the cellular level between thousands, if not millions, of cells within a single biological organ. Technological advances over the next decade will make it feasible to simulate these interactions on a computer, providing an invaluable tool for predicting how an organ behaves when presented with particular stimuli. Finite–element modelling techniques are particularly suited to this task, since, by dividing a system into a large number of small elements, they mimic the physical reality by which cell interactions, even over large distances, result from a large number of localized interactions between adjacent units. Finite–element techniques have been used in engineering for some time, and they are already being applied to a variety of biological organs. One example is the mammalian cochlea, where sound is transformed into electrical signals that are subsequently passed to the auditory nerve. The cochlea contains an amplifier of mechanical motion that operates on a microsecond time–scale at sub–nanometre displacements, and it enables the auditory system to respond over a dynamic range in excess of 120 dB. A simple finite–element model that represents the cochlea at a cellular level has already demonstrated the potential value of this approach by providing an explanation for contradictory experimental observations. Developing structurally realistic cell–level models of biological organs will improve our ability to properly characterize and quantify experimental observations, and dramatically reduce the need for animal experimentation. The finite–element approach could also provide a valuable tool in the design of new, simpler, cellular structures that would mimic the known operation of a biological organ. Given the impressive specifications of such organs, these new devices–manufactured in carbon or silicon–could have numerous research, clinical and industrial applications in the new millennium.
Two assumptions were made in the formulation of a recent cochlear model [P.J. Kolston, J. Acoust. Soc. Am. 83, 1481-1487 (1988)]: (1) The basilar membrane has two radial modes of vibration, corresponding to division into its arcuate and pectinate zones; and (2) the impedance of the outer hair cells (OHCs) greatly modifies the mechanics of the arcuate zone. Both of these assumptions are strongly supported by cochlear anatomy. This paper presents a revised version of the outer hair cell, arcuate-pectinate (OHCAP) model, which is an improvement over the original model in two important ways: First, a model for the OHCs is included so that the OHC impedance is no longer prescribed functionally; and, second, the presence of the OHCs enhances the basilar membrane motion, so that the model is now consistent with observed response changes resulting from trauma. The OHCAP model utilizes the unusual spatial arrangement of the OHCs, the Deiters cells, their phalangeal processes, and the pillars of Corti. The OHCs do not add energy to the cochlear partition and hence the OHCAP model is passive. In spite of the absence of active processes, the model exhibits mechanical tuning very similar to those measured by Sellick et al. [Hear. Res. 10, 93-100 (1983)] in the guinea pig cochlea and by Robles et al. [J. Acoust. Soc. Am. 80, 1364-1374 (1986)] in the chinchilla cochlea. Therefore, it appears that mechanical response tuning and response changes resulting from trauma should not be used as justifications for the hypothesis of active processes in the real cochlea.
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