@entity2421 ( @entity2421 ) 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 @entity63 is therefore disturbing. That stimulus intensities must exceed 50-60 dB @entity16811 for residual CDTs to be recorded and for level notches to be present in @entity2421 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 @entity2421 level and phase for 50 and 60 dB @entity16811 stimuli and group-delay measurements. After a clear initial decay, @entity2421 levels elicited at 60 dB @entity16811 plateaued for several minutes at about 20 dB below initial level, and when early level notches were observed, @entity2421 phase changes remained minor. The @entity2421 group delays decreased by less than 30%. Later @entity2421 level notches were associated with sharp phase reversals but the similarity between @entity2421 characteristics before and after a notch was hardly consistent with a two-component interpretation. When mild sound overexposure (pure tone, 90-95 dB @entity16811 , 15-30 min) had been performed prior to @entity63 , little or no ischemic @entity2421 came from the frequency bands where auditory fatigue had been detected (within 1 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 @entity2421 source related to mechano-electrical transduction in outer hair cells. More parsimonious than a two-component model, it posits that although early stages of @entity63 dramatically impair the overall performance of the cochlea, the nonlinear mechanical stages responsible for the existence of CDTs keep working albeit at higher intensities.

Origin of cubic difference tones generated by high-intensity stimuli: effect of XXXX and auditory fatigue on the gerbil cochlea.

@entity2421 :: ('MESH:D009123', 'Disease') :: ['Cubic difference tone', 'CDT'] @entity16811 :: ('8879', 'Gene') :: ['SPL'] @entity63 :: ('MESH:D007511', 'Disease') :: ['cochlear ischemia', 'ischemia']
@entity63 :: (MESH:D007511,Disease) :: ['ischemia']
