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报告题目:
Origin within the cochlea of otoacoustic emissions evoked by narrow-band stimuli
 报告人:
Siegel, Jonathan H., PhD
Associate Professor of Audiology 
Associate Professor of Neurobiology and Physiology 
Associate Professor of Otolaryngology
University of Northwestern University, USA
报告时间:
2012-09-04 15:00
报告地点:
清华大学医学科学院楼B-321
主办单位:
清华大学医学院
  简介:
       Otoacoustic emissions evoked from living ears by low-level tones (stimulus frequency otoacoustic emissions, or SFOAE) and narrow-band tone-pips (TEOAE) are commonly believed to originate by coherent linear reflection from the peak of the traveling wave near the place in the cochlea that resonates at the frequency of the stimulus.  However, evidence collected primarily from experiments in laboratory animals appears more compatible with a distributed generator model, in which hair cells at each place along the cochlear excitation pattern evoked by the stimulus contribute to the ear canal emission in a manner determined by the local amplitude and phase of the vibration.  Instead of emphasizing contributions from the peak region, as predicted by coherent linear reflection, the distributed generator model predicts that the contribution from the peak (short wave) region is reduced by destructive interference, while contributions from hair cells in more basal locations are emphasized due to the long wavelength of the basilar membrane traveling wave at locations basal to the peak. The strongest evidence in support of this alternative scheme comes from experiments in which hair cells in a restricted region of the cochlea are damaged by an intense tone, elevating compound neural thresholds by 30-40 dB, when measured using tone burst stimuli. SFOAE and TEOAE evoked by low-level tones and tone pips with frequencies centered in the “notch” in neural thresholds are not consistently reduced to a degree commensurate with the change in neural threshold.  On the other hand, changes in distortion-product otoacoustic emissions (DPOAE) evoked by simultaneously presenting two low-level stimulus tones, often match the change in neural thresholds much more closely.  Although the mechanisms of otoacoustic emissions appear less well understood than commonly believed, these experiments demonstrate that, with appropriately chosen stimuli, DPOAE originate in a much more restricted region of the cochlea than SFOAE and TEOAE evoked by low-level tones and tone-pips.  Apart from better understanding mechanisms of otoacoustic emissions, these findings are relevant to clinical assessment of damaged regions of the cochlea.
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