Title: Otoacoustic Emission Cochleography The planned research is designed to provide an improved understanding of the mechanisms underlying both the generation of DPOAEs as well as the key features of this emission's large, complex response space. This general aim is being accomplished by using DPOAE level/phase (L/P) maps that consider both DPOAE magnitude and phase as a function of f2/f1 ratio and DPOAE frequency. According to the commonly accepted 2-source model of DPOAE generation, in these maps, horizontal-phase banding (shallow phase slope vs fdp) is indicative of distortion-source emissions from the f2 place, while vertical-phase banding (steep phase slope vs fdp) signifies reflection emissions from the DPOAE-frequency place (fdp). Recently, we discovered that interference tones (ITs) placed near fdp in these maps were unable to remove all vertical-phase banding at higher primary-tone levels in humans, or to extract any DPOAE-reflection components in the presence of vertical-phase banding in rabbits.
Aim #1 investigates the hypothesis that vertical-phase banding refractory to ITs near fdp depends on primary-tone level, species, and SFOAEs. Thus, DPOAE L/P maps from rabbits, chinchillas, and humans collected with and without an IT near fdp at various f1 and f2 levels will be compared, and related to the presence of SFOAEs, a signature of the reflection mechanism. It is postulated that OAEs refractory to ITs near fdp arise from a distributed basal source of DPOAEs and therefore onset latencies of these emissions should be shorter than distortion emissions obtained for the same f2.
Aim #2 focuses on the hypothesis that depending upon primary-tone levels and species, DPOAE components extracted with IFFT methods may not match those revealed by IT techniques because, while both humans and rabbits exhibit shallow and steep phase-gradient DPOAE components, they differ in their response to ITs near fdp.
Aim #3 investigates the notion that a basal source of DPOAEs plays a substantial role in DPOAE residuals revealed by tones or bands of noise above f2. This source also acts to `fill in'regions of dysfunction as revealed by traditional DP-grams. The likelihood of this basal source will be investigated by determining the octave extent over which difference tones (f2-f1) can be produced for various levels of f1 and f2. Noisebands with increasingly higher low-frequency cutoffs with respect to f2 and ITs placed at successive 0.33-octave increments above f2 will be used to reveal abnormal residuals in DPOAE L/P maps following noise damage and help establish the presence and properties of a basal source of DPOAEs. Finally, DP-grams will be collected with and without an IT 0.33 octaves abovef2 in humans with 4-kHz noise-induced notches in their audiograms to determine if, as in rabbits, the true extent of the corresponding DP-gram notch is partially obscured by a basal DPOAE source. The planned studies promise to modify accepted wisdom regarding mechanisms of DPOAE generation, and may also lead to the development of DPOAE tests that are more useful by allowing accurate cochlear-damage patterns to be revealed at higher primary-tone levels where signal-to-noise ratios are notably improved.

Public Health Relevance

Otoacoustic Emission Cochleography The majority of our theoretical understanding of distortion product otoacoustic emissions is based on low-level acoustic stimulation. The proposed studies extend these efforts to more clinically relevant levels where basal generators appear to obscure cellular damage patterns. Understanding these mechanisms may eventually permit a more accurate depiction of the pattern of cochlear dysfunction with improved signal-to-noise ratios for clinic patients exhibiting particular hearing impairments.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC000613-25
Application #
8461234
Study Section
Auditory System Study Section (AUD)
Program Officer
Miller, Roger
Project Start
1989-04-01
Project End
2014-05-31
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
25
Fiscal Year
2013
Total Cost
$506,262
Indirect Cost
$165,834
Name
Loma Linda Veterans Assn Research & Education
Department
Type
DUNS #
606630762
City
Redlands
State
CA
Country
United States
Zip Code
92373
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
Bektas, Devrim; Martin, Glen K; Stagner, Barden B et al. (2008) Noise-induced hearing loss in mice treated with antiretroviral drugs. Hear Res 239:69-78
Martin, Glen K; Vazquez, Ana E; Jimenez, Ana M et al. (2007) Comparison of distortion product otoacoustic emissions in 28 inbred strains of mice. Hear Res 234:59-72

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