Distortion Product Otoacoustic Emissions in Mice Above and Below the Eliciting Primaries.

Abstract

Normal hearing is associated with cochlear nonlinearity. When two tones (f1 and f2) are presented, the intracochlear response contains additional components that can be recorded from the ear canal as distortion product otoacoustic emissions (DPOAEs). Although the most prominent intermodulation distortion component is at 2f1-f2, other cubic distortion products are also generated. Because these measurements are noninvasive, they are used in humans and in animal models to detect hearing loss. This study evaluated how loss of sensitivity affects DPOAEs with frequencies above and below the stimulating primaries, i.e., for upper sideband (USB) components like 2f2-f1 and for lower sideband (LSB) components like 2f1-f2. DPOAEs were recorded in several mouse mutants with varying degrees of hearing loss associated with structural changes to the tectorial membrane (TM), or with loss of outer hair cell (OHC) somatic electromotility due to lack of prestin or to the expression of a non-functional prestin. In mice with changes in sensitivity, magnitude reductions were observed for 2f1-f2 relative to controls with mice lacking prestin showing the greatest changes. In contrast, 2f2-f1 was minimally affected by reductions in cochlear gain due to changes in the TM or by the loss of OHC somatic electromotility. In addition, TM mutants with spontaneous otoacoustic emissions (SOAEs) generated larger responses than controls at 2f2-f1 when its frequency was similar to that for the SOAEs. Although cochlear pathologies appear to affect USB and LSB DPOAEs in different ways, both 2f1-f2 and 2f2-f1 reflect nonlinearities associated with the transducer channels. However, in mice, the component at 2f2-f1 does not appear to receive enhancement due to prestin's motor action.