The quantitative relation between sensory cell loss and hearing thresholds

Hamernik, Roger P.; Patterson, J. Herbert; Turrentine, George; Ahroon, William A.

doi:10.1016/0378-5955(89)90065-8

Cited by 126 publications

(60 citation statements)

References 19 publications

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“…In contrast, old-exposed ears show no threshold elevation. Similar results were obtained with ABR and DPOAE measures, consistent with the notion that the functionally important changes in these ears involve the outer hair cells, which are among the most vulnerable structures in the inner ear (Hamernik et al, 1989;Saunders et al, 1991;Dallos, 1992).…”

Section: Nihl Vulnerability Varies With Age At Exposuresupporting

confidence: 76%

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Kujawa¹,

Liberman²

2006

J. Neurosci.

595

411

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Age-related and noise-induced hearing losses in humans are multifactorial, with contributions from, and potential interactions among, numerous variables that can shape final outcome. A recent retrospective clinical study suggests an age-noise interaction that exacerbates age-related hearing loss in previously noise-damaged ears (Gates et al., 2000). Here, we address the issue in an animal model by comparing noise-induced and age-related hearing loss (NIHL; AHL) in groups of CBA/CaJ mice exposed identically (8 -16 kHz noise band at 100 dB sound pressure level for 2 h) but at different ages (4 -124 weeks) and held with unexposed cohorts for different postexposure times (2-96 weeks). When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4 -8 weeks) were 40 -50 dB; older-exposed animals (Ն16 weeks) showed essentially no shift at the same postexposure time. However, when held for long postexposure times, animals with previous exposure demonstrated AHL and histopathology fundamentally unlike unexposed, aging animals or old-exposed animals held for 2 weeks only. Specifically, they showed substantial, ongoing deterioration of cochlear neural responses, without additional change in preneural responses, and corresponding histologic evidence of primary neural degeneration throughout the cochlea. This was true particularly for young-exposed animals; however, delayed neuropathy was observed in all noise-exposed animals held 96 weeks after exposure, even those that showed no NIHL 2 weeks after exposure. Data suggest that pathologic but sublethal changes initiated by early noise exposure render the inner ears significantly more vulnerable to aging.

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Section: Nihl Vulnerability Varies With Age At Exposuresupporting

confidence: 76%

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Kujawa¹,

Liberman²

2006

J. Neurosci.

595

411

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“…For example, Kanamycin sulfate treatment, causing complete loss of OHCs, with preservation of IHCs, results in threshold shifts of 40 dB and more in chinchillas (Woolf et al, 1981). In the same species, the first approximate 30 dB of noise-exposure induced permanent threshold shifts is induced by primarily outer hair cell losses (Hamernik et al, 1989). On the other hand, neomycin in combination with acoustic trauma causes decreases in cochlear sensitivity amounting up to 62 dB, averaged across all frequencies, in guinea pigs with losses of cochlear OHCs close to 100% (Brown et al, 1978).…”

Section: Role Of Outer Hair Cells In Hearing Loss In Hdrmentioning

confidence: 99%

GATA3 haploinsufficiency causes a rapid deterioration of distortion product otoacoustic emissions (DPOAEs) in mice

Looij

Burg²,

Giessen³

et al. 2005

Neurobiology of Disease

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Human HDR (hypoparathyroidism, deafness and renal dysplasia)-syndrome is caused by haploinsufficiency of zinc-finger transcription factor GATA3. The hearing loss due to GATA3 haploinsufficiency has been shown to be peripheral in origin, but it is unclear to what extent potential aberrations in the outer hair cells (OHCs) contribute to this disorder. To further elucidate the pathophysiological mechanism underlying the hearing defect in HDR-syndrome, we investigated the OHCs in heterozygous Gata3-knockout mice at both the functional and morphological level. While the signal-to-noise ratios of distortion product otoacoustic emissions (DPOAE) in wild type mice did not change significantly during the first half-year of live, those in the heterozygous Gata3 mice decreased dramatically. In addition, both light microscopic and transmission electron microscopic analyses showed that the number of OHCs containing vacuoles was increased in the mutants. Together, these findings indicate that outer hair cell malfunctioning plays a major role in the hearing loss in HDR-syndrome. D

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“…Critical irreversible changes (those accounting for permanent hearing loss) have appeared concentrated in the organ of Corti. These include hair cell loss and non-lethal hair cell injury (e.g., Covell 1953;Johnson and Hawkins 1976;Hamernik et al 1989;Ou et al 2000b;Wang et al 2002) as well as newly recognized delayed and progressive injury to afferent neurons (Kujawa and Liberman 2009). The latter may not contribute to hearing loss per se, but rather to supra-threshold deficits.…”

Section: Introductionmentioning

confidence: 99%

Different Cellular and Genetic Basis of Noise-Related Endocochlear Potential Reduction in CBA/J and BALB/cJ Mice

Ohlemiller

Rosen

Rellinger

et al. 2010

JARO

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The acute and permanent effects of noise exposure on the endocochlear potential (EP) and cochlear lateral wall were evaluated in BALB/cJ (BALB) inbred mice, and compared with CBA/J (CBA) and C57BL/6 (B6) mice. Two-hour exposure to broadband noise (4-45 kHz) at 110 dB SPL leads to a~50 mV reduction in the EP in BALB and CBA, but not B6. EP reduction in BALB and CBA is reliably associated with characteristic acute cellular pathology in stria vascularis and spiral ligament. By 8 weeks after exposure, the EP in CBA mice has returned to normal. In BALBs, however, the EP remains depressed by an average~10 mV, so that permanent EP reduction contributes to permanent threshold shifts in these mice. We recently showed that the CBA noise phenotype in part reflects the influence of a large effect quantitative trait locus on Chr. 18, termed Nirep (Ohlemiller et al., Hear Res 260:47-53, 2010b). While CBA "EP susceptibility" alleles are dominant to those in B6, examination of (B6×BALB) F1 hybrid mice and (F1×BALB) N2 backcross mice revealed that noise-related EP reduction and associated cell pathology in BALBs are inherited in an autosomal recessive manner, and are dependent on multiple genes. Moreover, while N2 mice formed from B6 and CBA retain strong correspondence between acute EP reduction, ligament pathology, and strial pathology, N2s formed from B6 and BALB include subsets that dissociate pathology of ligament and stria. We conclude that the genes and cascades that govern the very similar EP susceptibility phenotypes in BALB and CBA mice need not be the same. BALBs appear to carry alleles that promote more pronounced long term effects of noise on the lateral wall. Separate loci in BALBs may preferentially impact stria versus ligament.

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The quantitative relation between sensory cell loss and hearing thresholds

Cited by 126 publications

References 19 publications

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

Acceleration of Age-Related Hearing Loss by Early Noise Exposure: Evidence of a Misspent Youth

GATA3 haploinsufficiency causes a rapid deterioration of distortion product otoacoustic emissions (DPOAEs) in mice

Different Cellular and Genetic Basis of Noise-Related Endocochlear Potential Reduction in CBA/J and BALB/cJ Mice

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