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Titolo:
Origin of cubic difference tones generated by high-intensity stimuli: Effect of ischemia and auditory fatigue on the gerbil cochlea
Autore:
Mom, T; Bonfils, P; Gilain, L; Avan, P;
Indirizzi:
Sch Med, Lab Sensory Biophys, EA 2667, F-63001 Clermont Ferrand, France Sch Med Clermont Ferrand France F-63001 F-63001 Clermont Ferrand, France Format Associee Claude Bernard, Lab Rech Audit, Paris, France Format Associee Claude Bernard Paris France b Rech Audit, Paris, France Hop Europeen Georges Pompidou, CNRS, UPRESA 7060, Paris, France Hop Europeen Georges Pompidou Paris France , UPRESA 7060, Paris, France
Titolo Testata:
JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA
fascicolo: 3, volume: 110, anno: 2001,
parte:, 1
pagine: 1477 - 1488
SICI:
0001-4966(200109)110:3<1477:OOCDTG>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRODUCT OTOACOUSTIC EMISSIONS; OUTER HAIR-CELLS; BASILAR-MEMBRANE NONLINEARITY; ACOUSTIC DISTORTION PRODUCTS; SENSORINEURAL HEARING-LOSS; TEMPORARY THRESHOLD SHIFT; 2 DISCRETE SOURCES; GUINEA-PIG; MECHANOELECTRICAL TRANSDUCER; LOUD SOUND;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Engineering, Computing & Technology
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Avan, P Sch Med, Lab Sensory Biophys, EA 2667, POB 38, F-63001 Clermont Ferrand, France Sch Med POB 38 Clermont Ferrand France F-63001 nt Ferrand, France
Citazione:
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

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 complete cochlear ischemia is therefore disturbing. That stimulus intensities must exceed 50-60 dB SPL for residual CDTs to be recorded and for level notches to be present in CDT growth functions is often cited as evidence for a two-component, "active/passive" model: one component, the residual one, would originate from a passive, hardly vulnerable mechanism and thus be unsuitable for hearing screening purposes. This model was probed in gerbil ears after complete interruption of the cochlear blood flow. Cochlear potentials and CDTs were controlled simultaneously through continuous monitoring of CDTlevel 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 notches were observed, CDT phase changes remained minor. The CDT group delays decreased by less than 30%. Later CDT level notches were associated withsharp phase reversals but the similarity between CDT characteristics before and after a notch was hardly consistent with a two-component interpretation. When mild sound overexposure (pure tone, 90-95 dB SPL, 15-30 min) had been performed prior to ischemia, little or no ischemic CDT came from the frequency bands where auditory fatigue had been detected (within I kHz), irrespective of the stimulus intensity. It suggests that instead of being passive, residual ischemic CDTs were vulnerable and produced according to a near-normal tonotopy by the same mechanisms that were sensitive to auditory fatigue. All the results lined up with a simple feedback model of cochlear function assuming a single CDT source related to mechano-electrical transduction in outer hair cells. More parsimonious than a two-component model, it posits that although early stages of ischemia dramatically impair the overallperformance of the cochlea, the nonlinear mechanical stages responsible for the existence of CDTs keep working albeit at higher intensities. (C) 2001Acoustical Society of America.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 14:22:08