The primary goal of the proposed experiments on distortion-produc otoacoustic emissions (DPOAEs) is to investigate more completely particular issues that impact the field's fundamental understanding of several relatively recently developed measures of suppression and latency. An additional aim is t begin to identify the anatomical counterparts of the DPOAE-generation process. Specifically, one explicit goal is to determine if suppression-tuning curves provide a measure of cochlear trauma, or indication of the DPOAE generation site(s). Another specific aim is to determine the contribution that basal oute hair cells (OHCs) make to the observations in small laboratory animals and humans of suppression and enhancement of the DPOAE above the Q place. A furthe aim is to establish if systematically induced changes in DPOAE latency measure reflect alterations in cochlear filtering and/or build-up of the DPOAE-generation process. A final specific aim is to begin to determine if the status of the OFIC's stereocilia contribute to the viability of high-level DPOAE generator, and if the altered suppression tuning exhibited by some experimental animals following noise exposure is associated with more basally located regions of normal OHCs. The proposed studies will be performed in a parallel manner using both human and laboratory-rabbit subjects. The basic experimental plan is to make critical comparisons between DPOAEs generated in normal and pathological ears that have been temporarily or permanently altered by either exposure to excessive sounds or the administration of the ototoxic drug furosemide. The results of the planned experiments will contribute to out knowledge base concerning the basic processes underlying the production of DPOAEs, the identity of DPOAE measures that promise to be clinically useful, and the relevance of DPOAE generation in laboratory mammals to that in humans.

National Institute of Health (NIH)
National Institute on Deafness and Other Communication Disorders (NIDCD)
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Hearing Research Study Section (HAR)
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Donahue, Amy
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University of Miami School of Medicine
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Martin, Glen K; Stagner, Barden B; Dong, Wei et al. (2016) Comparing Distortion Product Otoacoustic Emissions to Intracochlear Distortion Products Inferred from a Noninvasive Assay. J Assoc Res Otolaryngol 17:271-87
Luebke, Anne E; Stagner, Barden B; Martin, Glen K et al. (2015) Influence of sound-conditioning on noise-induced susceptibility of distortion-product otoacoustic emissions. J Acoust Soc Am 138:58-64
Luebke, Anne E; Stagner, Barden B; Martin, Glen K et al. (2014) Adaptation of distortion product otoacoustic emissions predicts susceptibility to acoustic over-exposure in alert rabbits. J Acoust Soc Am 135:1941-9
Martin, Glen K; Stagner, Barden B; Lonsbury-Martin, Brenda L (2013) Time-domain demonstration of distributed distortion-product otoacoustic emission components. J Acoust Soc Am 134:342-55
Gratton, Michael Anne; Eleftheriadou, Anna; Garcia, Jerel et al. (2011) Noise-induced changes in gene expression in the cochleae of mice differing in their susceptibility to noise damage. Hear Res 277:211-26
Martin, Glen K; Stagner, Barden B; Chung, You Sun et al. (2011) Characterizing distortion-product otoacoustic emission components across four species. J Acoust Soc Am 129:3090-103
Martin, Glen K; Stagner, Barden B; Lonsbury-Martin, Brenda L (2010) Evidence for basal distortion-product otoacoustic emission components. J Acoust Soc Am 127:2955-72
Martin, Glen K; Stagner, Barden B; Fahey, Paul F et al. (2009) Steep and shallow phase gradient distortion product otoacoustic emissions arising basal to the primary tones. J Acoust Soc Am 125:EL85-92
McFadden, Dennis; Martin, Glen K; Stagner, Barden B et al. (2009) Sex differences in distortion-product and transient-evoked otoacoustic emissions compared. J Acoust Soc Am 125:239-46
Fahey, P F; Stagner, B B; Martin, G K (2008) Source of level dependent minima in rabbit distortion product otoacoustic emissions. J Acoust Soc Am 124:3694-707

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