Transmission of oto-acoustic emissions within the cochlea.
ABSTRACT Oto-acoustic emissions (OAEs) are low intensity sounds which can be recorded in the external ear canal with a sensitive microphone. They are initiated by the activated motility of the outer hair cells which provide mechanical feedback (the cochlear amplifier) to the basilar membrane, enhancing its displacement. Therefore it has been thought that the OAEs are propagated toward the base as a backward mechanical traveling wave along the basilar membrane. Such a wave would be accompanied by pressure differences across the cochlear partition in the closed cochlear system, filled with incompressible fluid. In order to test this OAE propagation mechanism, holes were made in several places in the bony wall of the inner ear, reducing such possible pressure differences. In experiments in which it was possible to avoid damage to the organ of Corti, there was no change in detection thresholds of distortion product OAEs. This result provides further support for the suggestion that oto-acoustic emissions are not propagated as mechanical vibrations backward along the basilar membrane. Instead it is more likely that they are transmitted through the cochlear fluids to the stapes footplate as alternating condensation/ rarefaction fluid pressures.
Clinical Neurophysiology 06/2006; 117(5):933-4. DOI:10.1016/j.clinph.2006.01.001 · 2.98 Impact Factor
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ABSTRACT: The equality of volume displacements in the inner ear windows is commonly assumed. In the present work this assumption is experimentally verified. The stapes is given a known displacement. The volume displacement of the round window is determined by measuring the sound pressure set up in a tube cemented to the round window. Inner ears of pigs have been used in the investigation. Supplementary measurements on one human temporal bone have been performed. The equality of the volume flows in the inner ear windows is also supported through an analysis of earlier measurements of the round window displacement for a given sound-pressure level at the eardrum.The Journal of the Acoustical Society of America 08/1995; 98(1):192-6. DOI:10.1121/1.413746 · 1.56 Impact Factor
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ABSTRACT: In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.Journal of basic and clinical physiology and pharmacology 02/2004; 15(1-2):1-14. DOI:10.1515/JBCPP.2004.15.1-2.1