Origin of cubic difference tones generated by high-intensity stimuli: Effect of ischemia and auditory fatigue on the gerbil cochlea

Citation
T. Mom et al., Origin of cubic difference tones generated by high-intensity stimuli: Effect of ischemia and auditory fatigue on the gerbil cochlea, J ACOUST SO, 110(3), 2001, pp. 1477-1488
Citations number
61
Categorie Soggetti
Multidisciplinary,"Optics & Acoustics
Journal title
JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA
ISSN journal
00014966 → ACNP
Volume
110
Issue
3
Year of publication
2001
Part
1
Pages
1477 - 1488
Database
ISI
SICI code
0001-4966(200109)110:3<1477:OOCDTG>2.0.ZU;2-5
Abstract
Cubic difference tone (CDT) otoacoustic emissions are thought to arise from the feedback loop allowing outer hair cells to enhance the sensitivity and tuning of the organ of Corti. The existence of residual CDTs during comple te cochlear ischemia is therefore disturbing. That stimulus intensities mus t exceed 50-60 dB SPL for residual CDTs to be recorded and for level notche s to be present in CDT growth functions is often cited as evidence for a tw o-component, "active/passive" model: one component, the residual one, would originate from a passive, hardly vulnerable mechanism and thus be unsuitab le for hearing screening purposes. This model was probed in gerbil ears aft er complete interruption of the cochlear blood flow. Cochlear potentials an d CDTs were controlled simultaneously through continuous monitoring of CDT level and phase for 50 and 60 dB SPL stimuli and group-delay measurements. After a clear initial decay, CDT levels elicited at 60 dB SPL plateaued for several minutes at about 20 dB below initial level, and when early level n otches were observed, CDT phase changes remained minor. The CDT group delay s decreased by less than 30%. Later CDT level notches were associated with sharp phase reversals but the similarity between CDT characteristics before and after a notch was hardly consistent with a two-component interpretatio n. When mild sound overexposure (pure tone, 90-95 dB SPL, 15-30 min) had be en performed prior to ischemia, little or no ischemic CDT came from the fre quency bands where auditory fatigue had been detected (within I kHz), irres pective of the stimulus intensity. It suggests that instead of being passiv e, residual ischemic CDTs were vulnerable and produced according to a near- normal tonotopy by the same mechanisms that were sensitive to auditory fati gue. All the results lined up with a simple feedback model of cochlear func tion assuming a single CDT source related to mechano-electrical transductio n in outer hair cells. More parsimonious than a two-component model, it pos its that although early stages of ischemia dramatically impair the overall performance of the cochlea, the nonlinear mechanical stages responsible for the existence of CDTs keep working albeit at higher intensities. (C) 2001 Acoustical Society of America.