Experimental data on the mechanical properties of the tissues of the mammalian cochlea are essential for understanding the frequency- and location-dependent motion patterns that result in response to incoming sound waves. Within the cochlea, sound-induced vibrations are transduced into neural activity by the organ of Corti, the gross motion of which is dependent on the motion of the underlying basilar membrane. In this study we present data on stiffness of the gerbil basilar membrane measured at multiple positions within a cochlear cross section and at multiple locations along the length of the cochlea. A basic analysis of these data using relatively simple models of cochlear mechanics reveals our most important result: the experimentally measured longitudinal stiffness gradient at the middle of the pectinate zone of the basilar membrane (4.43 dB/mm) can account for changes of best frequency along the length of the cochlea. Furthermore, our results indicate qualitative changes of stiffness-deflection curves as a function of radial position; in particular, there are differences in the rate of stiffness growth with increasing tissue deflection. Longitudinal coupling within the basilar membrane/organ of Corti complex is determined to have a space constant of 21 microm in the middle turn of the cochlea. The bulk of our data was obtained in the hemicochlea preparation, and we include a comparison of this set of data to data obtained in vivo.

Most cochlear implant strategies utilize monopolar stimulation, likely inducing relatively broad activation of the auditory neurons. The spread of activity may be narrowed with a tripolar stimulation scheme, wherein compensating current of opposite polarity is simultaneously delivered to two adjacent electrodes. In this study, a model and cochlear implant subjects were used to examine loudness growth for varying amounts of tripolar compensation, parameterized by a coefficient sigma, ranging from 0 (monopolar) to 1 (full tripolar). In both the model and the subjects, current required for threshold activation could be approximated by I(sigma)=Ithr(0)(1-sigmaK), with fitted constants Ithr(0) and K. Three of the subjects had a "positioner," intended to place their electrode arrays closer to their neural tissue. The values of K were smaller for the positioner users and for a "close" electrode-to-tissue distance in the model. Above threshold, equal-loudness contours for some subjects deviated significantly from a linear scale-up of the threshold approximations. The patterns of deviation were similar to those observed in the model for conditions in which most of the neurons near the center electrode were excited.

The mammalian inner ear processes sound with high sensitivity and fine resolution over a wide frequency range. The underlying mechanism for this remarkable ability is the "cochlear amplifier", which operates by modifying cochlear micromechanics. However, it is largely unknown how the cochlea implements this modification. Although gradual improvements in experimental techniques have yielded ever-better descriptions of gross basilar membrane vibration, the internal workings of the organ of Corti and of the tectorial membrane have resisted exploration. Although measurements of cochlear function in mice with a gene mutation for alpha-tectorin indicate the tectorial membrane's key role in the mechanoelectrical transformation by the inner ear, direct experimental data on the tectorial membrane's physical properties are limited, and only a few direct measurements on tectorial micromechanics are available. Using the hemicochlea, we are able to show that a tectorial membrane stiffness gradient exists along the cochlea, similar to that of the basilar membrane. In artificial perilymph (but with low calcium), the transversal and radial driving point stiffnesses change at a rate of -4.0 dB/mm and -4.9 dB/mm, respectively, along the length of the cochlear spiral. In artificial endolymph, the stiffness gradient for the transversal component was -3.4 dB/mm. Combined with the changes in tectorial membrane dimensions from base to apex, the radial stiffness changes would be able to provide a second frequency-place map in the cochlea. Young's modulus, which was obtained from measurements performed in the transversal direction, decreased by -2.6 dB/mm from base to apex.

This report describes stiffness and best frequency measurements obtained in vitro from the basilar membrane of the gerbil cochlea at the onset of hearing, during hearing maturation, and after hearing has matured. Our stiffness data constitute the first direct experimental evidence of developmental stiffness changes in the basal and middle turns. Stiffness changes by a factor of 5.5 in the basal turn between postnatal day 11 and adult, and the difference from adult is statistically significant for all ages measured up to postnatal day 16. For the middle turn, stiffness changes by a factor of 1.6 between postnatal day 11 and adult. Whereas for postnatal day 12 and beyond there is no statistically significant difference from adult, our data suggest that there may be a significant difference of stiffness between day 11 and adult in the middle turn. For the basal turn, our motion measurements confirm a passive component to the developmental best frequency shift. For the middle turn, changes in best frequency are not statistically significant. Best frequency was determined by stimulating the tissue at audio frequencies with a glass paddle and measuring motion with a computer-based imaging system. Tissue stiffness was measured with a piezoelectric-based sensor system. Tissue stiffness changes have previously been postulated to contribute to the best frequency shift observed in the cochlear base. Incorporating our data into a simple spring-mass resonance model demonstrates that our experimentally measured stiffness change can account for the change of best frequency. These results suggest that a stiffness change is, in fact, a critical component of the best frequency shift observed in the basal turn of the gerbil cochlea after the onset of hearing.