Abstract
The global standing-wave model for generation of spontaneous otoacoustic emissions (SOAEs) suggests that they are amplitude-stabilized standing waves and that the spacing between SOAEs corresponds to the interval over which the phase changes by one cycle as determined from the phase-gradient delays of stimulus frequency otoacoustic emissions (SFOAEs). Because data characterizing the relationship between spontaneous and evoked emissions in nonhuman mammals are limited, we examined SOAEs and SFOAEs in tectorial membrane (TM) mutants and their controls. Computations indicate that the spacing between adjacent SOAEs is predicted by the SFOAE phase-gradient delays for TM mutants lacking Ceacam16, where SOAE frequencies are greater than ~20 kHz and the mutants retain near-normal hearing when young. Mice with a missense mutation in Tecta (TectaY1870C/+), as well as mice lacking Otoancorin (Otoa−/−), were also examined. Although these mutants exhibit hearing loss, they generate SOAEs with average frequencies of 11 kHz in TectaY1870C/+ and 6 kHz in Otoa−/−. In these animals, the spacing between adjacent SOAEs is larger than predicted by the SFOAE phase delays. It is also demonstrated that mice do not exhibit the strong frequency-dependence in signal coding that characterizes species with good low-frequency hearing. In fact, a transition occurs near the apical end of the mouse cochlea rather than at the mid-point along the cochlear partition. Hence, disagreements with the standing-wave model are not easily explained by a transition in tuning ratios between apical and basal regions of the cochlea, especially for SOAEs generated in TectaY1870C/+mice.
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