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Growth of suppression using distortion-product otoacoustic emission measurements in hearing-impaired humans.

ABSTRACT: Growth of distortion-product otoacoustic emission suppression was measured in 65 subjects with mild-to-moderate sensorineural hearing loss (HI). Measurements were made at four probe frequencies (f(2)) and up to five L(2) levels. Eleven suppressor frequencies (f(3)) were used for each f(2), L(2) combination. These data were compared to data from normal-hearing (NH) subjects (Gorga et al., 2011a). In both NH and HI subjects, growth of suppression depended on the relation between f(2) and f(3), such that the slope was close to one when f(3) ≈ f(2), steeper than one when f(3) < f(2), and shallower than one when f(3) > f(2). Differences in growth of suppression between NH and HI subjects were not observed for fixed f(2), L(2) combinations, however large differences were observed in suppressor "threshold" when compared at the same probe sensation level (dB SL). Smaller group differences were observed when compared at the same probe sound-pressure level (dB SPL). Therefore, the extent of these differences depended on how probe level (L(2)) was specified. When the results from NH and HI subjects are compared with each other and with psychophysical studies of masking, differences are observed that have implications for the remediation of mild-to-moderate hearing loss.

SUBMITTER: Birkholz C

PROVIDER: S-EPMC3505206 | biostudies-other | 2012 Nov

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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Growth of suppression using distortion-product otoacoustic emission measurements in hearing-impaired humans.

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