Cellular correlates of age-related endocochlear potential reduction in a mouse model

Ohlemiller, Kevin K.; Lett, Jaclynn M.; Gagnon, Patricia M.

doi:10.1016/j.heares.2006.06.012

Cited by 72 publications

(48 citation statements)

References 74 publications

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“…We measured the EP from the basal turn of six WT mice at P60. The mean magnitude was 94 ± 3.9 mV, consistent with previous EP values for mice [36]. Interestingly, the EP of Atoh1 -CKO mice was ~110 mV (right panel of Fig 3A), with a mean magnitude of 113 ± 4.8 mV (n = 6).…”

Section: Resultssupporting

confidence: 88%

Organ of Corti and Stria Vascularis: Is there an Interdependence for Survival?

Liu

Chen

et al. 2016

PLoS ONE

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Cochlear hair cells and the stria vascularis are critical for normal hearing. Hair cells transduce mechanical stimuli into electrical signals, whereas the stria is responsible for generating the endocochlear potential (EP), which is the driving force for hair cell mechanotransduction. We questioned whether hair cells and the stria interdepend for survival by using two mouse models. Atoh1 conditional knockout mice, which lose all hair cells within four weeks after birth, were used to determine whether the absence of hair cells would affect function and survival of stria. We showed that stria morphology and EP remained normal for long time despite a complete loss of all hair cells. We then used a mouse model that has an abnormal stria morphology and function due to mutation of the Mitf gene to determine whether hair cells are able to survive and transduce sound signals without a normal electrochemical environment in the endolymph. A strial defect, reflected by missing intermediate cells in the stria and by reduction of EP, led to systematic outer hair cell death from the base to the apex after postnatal day 18. However, an 18-mV EP was sufficient for outer hair cell survival. Surprisingly, inner hair cell survival was less vulnerable to reduction of the EP. Our studies show that normal function of the stria is essential for adult outer hair cell survival, while the survival and normal function of the stria vascularis do not depend on functional hair cells.

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Section: Resultssupporting

confidence: 88%

Organ of Corti and Stria Vascularis: Is there an Interdependence for Survival?

Liu

Chen

et al. 2016

PLoS ONE

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“…Mouse strains, however, also differ in the stability of the EP. In BALB/cJ and CBA/CaJ mice, the EP progressively declines with age, while C57/ BL and CBA/J mice largely maintain their EP (Ohlemiller et al, 2006). The EP in the CBA/J mouse in our study is also independent of age, commensurate with the largely normal appearance of stria vascularis.…”

Section: Stable Endocochlear Potentialsupporting

confidence: 65%

Age-related auditory pathology in the CBA/J mouse

et al. 2008

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Commercially obtained aged male CBA/J mice presented a complex pattern of hearing loss and morphological changes. A significant threshold shift in auditory brainstem responses (ABR) occurred at 3 months of age at 4 kHz without apparent loss of hair cells, rising slowly at later ages accompanied by loss of apical hair cells. A delayed high-frequency deficit started at 24 kHz around the age of 12 months. At 20 to 26 months, threshold shifts at 12 and 24 kHz and the accompanying hair cell loss at the base of the cochlea were highly variable with some animals appearing almost normal and others showing large deficits. Spiral ganglion cells degenerated by 18 months in all regions of the cochlea, with cell density reduced by approximately 25%. There was no degeneration of the stria vascularis and the endocochlear potential remained stable from 3 to 25 months of age regardless of whether the animals had normal or highly elevated ABR thresholds. The slow high frequency hearing loss combined with a modest reduction of ganglion cell density and an unchanged endocochlear potential suggest sensorineural presbycusis. The superimposed early hearing loss at low frequencies, which is not seen in animals bred in-house, may complicate the use of these animals as a presbycusis model.

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“…14). We previously used a single location approach to demonstrate mouse strain differences in age-related pathology of the cochlear lateral wall (Ohlemiller et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Genetic dependence of cochlear cells and structures injured by noise

Ohlemiller¹,

Gagnon²

2007

Hearing Research

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The acute and permanent effects of a single damaging noise exposure were compared in CBA/J, C57BL/6 (B6), and closely related strains of mice. Two hrs of broadband noise (4-45 kHz) at 110 dB SPL led to temporary reduction in the endocochlear potential (EP) of CBA/J and CBA/CaJ (CBA) mice and acute cellular changes in cochlear stria vascularis and spiral ligament. For the same exposure, B6 mice showed no EP reduction and little of the pathology seen in CBA. Eight weeks after exposure, all mice showed a normal EP, but only CBA mice showed injury and cell loss in cochlear lateral wall, despite the fact that B6 sustained larger permanent threshold shifts. Examination of noise injury in B6 congenics carrying alternate alleles of genes encoding otocadherin (Cdh23), agouti protein, and tyrosinase (albinism) indicated that none of these loci can account for the strain differences observed. Examination of B6xCBA F1 mice and F1xB6 N2 mice further indicated that susceptibility to noise-related EP reduction and associated cell pathology are inherited in an autosomal dominant manner, and are established by one or a few large effect quantitative trait loci. Findings support a common genetic basis for an entire constellation of noise related cochlear pathologies in cochlear lateral wall and spiral limbus. Even within species, cellular targets of acute and permanent cochlear noise injury may vary with genetic makeup.

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Cellular correlates of age-related endocochlear potential reduction in a mouse model

Cited by 72 publications

References 74 publications

Organ of Corti and Stria Vascularis: Is there an Interdependence for Survival?

Organ of Corti and Stria Vascularis: Is there an Interdependence for Survival?

Age-related auditory pathology in the CBA/J mouse

Genetic dependence of cochlear cells and structures injured by noise

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