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Considering distortion product otoacoustic emission fine structure in measurements of the medial olivocochlear reflex.

ABSTRACT: In humans, when the medial olivocochlear (MOC) pathway is activated by noise in the opposite ear, changes in distortion product otoacoustic emission (DPOAE) level, i.e., the MOC reflex, can be recorded in the test ear. Recent evidence suggests that DPOAE frequency influences the direction (suppression/enhancement) of the reflex. In this study, DPOAEs were recorded at fine frequency intervals from 500 to 2500 Hz, with and without contralateral acoustic stimulation (CAS) in a group of 15 adults. The MOC reflex was calculated only at DPOAE frequencies corresponding to peaks in the fine structure. Additionally, inverse fast-Fourier transform was conducted to evaluate MOC effects on individual DPOAE components. Results show the following: (1) When considering peaks only, the mean MOC reflex was -2.05 dB and 97% of observations reflected suppression, (2) CAS reduced distortion characteristic frequency component levels more than overlap component levels, and (3) CAS produced an upward shift in fine structure peak frequency. Results indicate that when the MOC reflex is recorded at DPOAE frequencies corresponding to fine structure maxima (i.e., when DPOAE components are constructive and in phase), suppression is reliably observed and level enhancement, which probably reflects component mixing in the ear canal rather than strength of the MOC reflex, is eliminated.

SUBMITTER: Abdala C

PROVIDER: S-EPMC2736726 | biostudies-other | 2009 Mar

REPOSITORIES: biostudies-other

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Project description:BackgroundAlthough several candidate-gene association studies have been conducted to investigate noise-induced hearing loss (NIHL) in humans, most are underpowered, unreplicated, and account for only a fraction of the genetic risk. Mouse genome-wide association studies (GWASs) have revolutionized the field of genetics and have led to the discovery of hundreds of genes involved in complex traits. The hybrid mouse diversity panel (HMDP) is a collection of classic inbred and recombinant inbred strains whose genomes have been either genotyped at high resolution or sequenced. To further investigate the genetics of NIHL, we report the first GWAS based on distortion product otoacoustic emission (DPOAE) measurements and the HMDP.MethodsA total of 102 strains (n = 635) from the HMDP were evaluated based on DPOAE suprathreshold amplitudes before and after noise exposure. DPOAE amplitude variation was set at 60 and 70 dB SPL of the primary tones for each frequency separately (8, 11.3, 16, 22.6, and 32 kHz). These values provided an indirect assessment of outer hair cell integrity. Six-week-old mice were exposed for 2 h to 10 kHz octave-band noise at 108 dB SPL. To perform local expression quantitative trait locus (eQTL) analysis, gene expression microarray profiles were generated using cochlear RNA from 64 hybrid mouse strains (n = 3 arrays per strain).ResultsSeveral new loci were identified and positional candidate-genes associated with NIHL were prioritized, especially after noise exposure (1 locus at baseline and 5 loci after exposure). A total of 35 candidate genes in these 6 loci were identified with at least 1 probe whose expression was regulated by a significant cis-eQTL in the cochlea. After careful analysis of the candidate genes based on cochlear gene expression, 2 candidate genes were prioritized: Eya1 (baseline) and Efr3a (post-exposure).Discussion and conclusionFor the first time, an association analysis with correction for population structure was used to map several loci for hearing traits in inbred strains of mice based on DPOAE suprathreshold amplitudes before and after noise exposure. Our results identified a number of novel loci and candidate genes for susceptibility to NIHL, especially the Eya1 and Efr3a genes. Our findings validate the power of the HMDP for detecting NIHL susceptibility genes.

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Considering distortion product otoacoustic emission fine structure in measurements of the medial olivocochlear reflex.

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