Genetic basis for susceptibility to noise-induced hearing loss in mice

Davis, Roger T.; Newlander, J. Kelly; Lei, Xiao; Cortopassi, Gino A; Krieg, Edward F.; Erway, Lawrence C.

doi:10.1016/s0378-5955(01)00250-7

Cited by 157 publications

(110 citation statements)

References 17 publications

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“…The use of B6 mice, which carry the Cdh23 ahl allele, may have impacted our results, insofar as this allele increases the extent of noise injury, and Cdh23 may bind calcium (Davis et al, 2001(Davis et al, ,2003. It is possible that our results will prove specific to B6 mice.…”

Section: Consideration Of the Animal Modelmentioning

confidence: 99%

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

et al. 2007

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Cochlear noise injury is the second most frequent cause of sensorineural hearing loss, after aging. Because calcium dysregulation is a widely recognized contributor to noise injury, we examined the potential of calcium channel blockers to reduce noise-induced hearing loss (NIHL) in mice. We focused on two T-type calcium blockers, trimethadione and ethosuximide, which are anti-epileptics approved by the Food and Drug Administration. Young C57BL/6 mice of either gender were divided into three groups: a 'prevention' group receiving the blocker via drinking water before noise exposure; a 'treatment' group receiving the blocker via drinking water after noise exposure; and controls receiving noise alone. Trimethadione significantly reduced NIHL when applied before noise exposure, as determined by auditory brainstem recording. Both ethosuximide and trimethadione were effective in reducing NIHL when applied after noise exposure. Results were influenced by gender, with males generally receiving greater benefit than females. Quantitation of hair cell and neuronal density suggested that preservation of outer hair cells could account for the observed protection. Immunocytochemistry and RT-PCR suggested that this protection involves direct action of T-type blockers on α1 subunits comprising one or more Ca v 3 calcium channel types in the cochlea. Our findings provide a basis for clinical studies testing T-type calcium blockers both to prevent and treat NIHL.

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Section: Consideration Of the Animal Modelmentioning

confidence: 99%

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

et al. 2007

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“…The ahl locus, responsible for age-related hearing loss and increased susceptibility to noise-induced hearing loss in C57BL/6 mice, has been mapped to chromosome 10 (Erway et al 1996;Johnson et al 1997Johnson et al , 2000Davis et al 2001). The position of this locus overlaps that of Cdh23 and it has been proposed that they may be allelic .…”

Section: Age-related Hearing Lossmentioning

confidence: 99%

Progressive Hearing Loss and Increased Susceptibility to Noise-Induced Hearing Loss in Mice Carrying a Cdh23 but not a Myo7a Mutation

Holme

Steel

2004

JARO - Journal of the Association for Research in Otolaryngolog

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Exposure to intense noise can damage the stereocilia of sensory hair cells in the inner ear. Since stereocilia play a vital role in the transduction of sound from a mechanical stimulus into an electrical one, this pathology is thought to contribute to noise-induced hearing loss. Mice homozygous for null mutations in either the myosin VIIa (Myo7a) or cadherin 23 (Cdh23) genes are deaf and have disorganized stereocilia bundles. We show that mice heterozygous for a presumed null allele of Cdh23 (Cdh23 v ) have low-and high-frequency hearing loss at 5-6 weeks of age, the high-frequency component of which worsens with increasing age. We also show that noise-induced hearing loss in 11-12-week-old Cdh23 v heterozygotes is two times greater than for wild-type littermates. Interestingly, these effects are dependent upon the genetic background on which the Cdh23 v mutation is carried. Noise-induced hearing loss in 11-12-week-old mice heterozygous for a null allele of Myo7a (Myo7a 4626SB ) is not significantly different from wildtype littermates. CDH23 is the first gene known to cause deafness in the human population to be linked with predisposition to noise-induced hearing loss.

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“…Since mice that carry the same allele typically show hearing loss early in adulthood, long before they are``old,'' the premise of such research is that Ahl accelerates cochlear degeneration that should also be observable in some aging mice. In C57BL/6 and BALB/c mice, Ahl also imparts susceptibility to noise injury (Henry 1982;Li 1992a;Erway et al 1996;Ohlemiller et al 2000b;Davis et al 2001;Jimenez et al 2001). This suggests that it accelerates a general aging-like process that is exquisitely sensitive to genetic and environmental interplay.…”

Section: Mouse Ahl As a Model For Human Arhlmentioning

confidence: 99%

“…C57BL/6-and BALB/c-related strains (henceforth C57BL/6 and BALB/c) are homozygous for Ahl (Johnson et al 1997(Johnson et al , 2000, which imparts both vulnerability to noise and ARHL (Henry 1982;Li 1992a;Erway et al 1996;Ohlemiller et al 2000b;Davis et al 2001;Jimenez et al 2001). Ahl may therefore exemplify a single locus that can promote mixed ARHL through a susceptibility mechanism (Li 1992b;Ohlemiller et al 2000a).…”

Section: Introductionmentioning

confidence: 99%

Reduction in Sharpness of Frequency Tuning but not Endocochlear Potential in Aging and Noise-Exposed BALB/cJ Mice

Ohlemiller

2002

JARO - Journal of the Association for Research in Otolaryngolog

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Schuknecht proposed categories for human age-related hearing loss (ARHL) based upon whether the primary degeneration involves the organ of Corti (sensory ARHL), spiral ganglion cells (neural), stria vascularis (strial), or a combination of these (mixed). Genetically standardized mouse ARHL models can help validate Schuknecht's framework and clarify the underlying cellular processes. Much recent work has focused on the mouse Ahl locus, which promotes both ARHL and noise-induced hearing loss. On the C57BL/6 inbred background, Ahl has been associated with degeneration of organ of Corti, afferent neurons, and stria vascularis/spiral ligament, suggesting that it promotes mixed (sensory/neural/strial) ARHL. Some cochlear degeneration in C57BL/6 mice could be caused by genes other than Ahl, however. The question of what constitutes Ahl-related pathology can be addressed by comparing C57BL/6 mice with other strains that carry the same allele, including BALB/c substrains. We examined the effects of aging and broadband noise exposure in inbred BALB/cJ mice (1.5±13.0 mos) using measures of frequency tuning (compound action potential tuning curves) (CAPTCs), strial function (endocochlear potential recording, EP), and light microscopy. Aging and noise led to generally similar physiological and anatomical changes. Reductions in sensitivity and sharpness of frequency tuning were not consistently linked to hair cell loss, reduction in the EP, or changes in the lateral wall. Instead they appeared best explained by alterations in supporting cells in the basal half of the cochlear and in the spiral limbus in the apex. These results emphasize the importance of cell types other than hair cells in cochlear pathology. They also indicate that Ahl does not necessarily promote a strial form of ARHL.

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Genetic basis for susceptibility to noise-induced hearing loss in mice

Cited by 157 publications

References 17 publications

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

Prophylactic and therapeutic functions of T-type calcium blockers against noise-induced hearing loss

Progressive Hearing Loss and Increased Susceptibility to Noise-Induced Hearing Loss in Mice Carrying a Cdh23 but not a Myo7a Mutation

Reduction in Sharpness of Frequency Tuning but not Endocochlear Potential in Aging and Noise-Exposed BALB/cJ Mice

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