Comparison of the Quantity of Cochlear Melanin in Young and Old C57BL/6 Mice

Hayashi, Hideo; Schachern, Patricia A.; Wakamatsu, Kazumasa; Paparella, Michael M.; Nakashima, Tsutomu

doi:10.1001/archotol.133.2.151

Cited by 18 publications

(15 citation statements)

References 35 publications

(37 reference statements)

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“…S9) is a transporter protein that has an important role in melanin synthesis15 and was recently reported to be one of the most abundantly expressed genes in the inner ear16. Melanin is highly sound-absorbing17 and may function in the inner ear to protect the cochlea from aging-related hearing loss and sound stressors in much the same manner as melanin in the skin protects against ultraviolet light181920. A recent study found that RGS7BP (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Genome analysis reveals insights into physiology and longevity of the Brandt’s bat Myotis brandtii

et al. 2013

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Bats account for one-fifth of mammalian species, are the only mammals with powered flight, and are among the few animals that echolocate. The insect-eating Brandt’s bat (Myotis brandtii) is the longest-lived bat species known to date (lifespan exceeds 40 years) and, at 4–8 g adult body weight, is the most extreme mammal with regard to disparity between body mass and longevity. Here we report sequencing and analysis of the Brandt’s bat genome and transcriptome, which suggest adaptations consistent with echolocation and hibernation, as well as altered metabolism, reproduction and visual function. Unique sequence changes in growth hormone and insulin-like growth factor 1 receptors are also observed. The data suggest that an altered growth hormone/insulin-like growth factor 1 axis, which may be common to other long-lived bat species, together with adaptations such as hibernation and low reproductive rate, contribute to the exceptional lifespan of the Brandt’s bat.

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Section: Resultsmentioning

confidence: 99%

Genome analysis reveals insights into physiology and longevity of the Brandt’s bat Myotis brandtii

et al. 2013

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“…In the stria, melanosomes are taken up by marginal and basal cells and fuse with lysosomes, where melanin deposits can remain indefinitely (Riley, 1997). In old mice, marginal cells are nearly outlined by dense melanin content (Hayashi et al, 2007; Ohlemiller et al, 2009), potentially reflecting an adaptive process. Among strial cells, marginal cells express an especially wide array of ion channels, transporters, and ATP-consuming pumps.…”

Section: Insights From Key Animal Modelsmentioning

confidence: 99%

Mechanisms and genes in human strial presbycusis from animal models

2009

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Schuknecht proposed a discrete form of presbycusis in which hearing loss results principally from degeneration of cochlear stria vascularis and decline of the endocochlear potential (EP). This form was asserted to be genetically linked, and to arise independently from age-related pathology of either the organ of Corti or cochlear neurons. Although extensive strial degeneration in humans coincides with hearing loss, EPs have never been measured in humans, and age-related EP reduction has never been verified. No human genes that promote strial presbycusis have been identified, nor is its pathophysiology well understood. Effective application of animal models to this issue requires models demonstrating EP decline, and preferably, genetically distinct strains that vary in patterns of EP decline and its cellular correlates. Until recently, only two models, Mongolian gerbils and Tyrp1 B-lt mice, were known to undergo age-associated EP reduction. Detailed studies of seven inbred mouse strains have now revealed three strains (C57BL/6J, B6.CAST-Cdh23 CAST , CBA/J) showing essentially no EP decline with age, and four strains ranging from modest to severe EP reduction (C57BL/6-Tyr c-2J , BALB/cJ, CBA/CaJ, NOD.NON-H2 nbl /LtJ). Collectively, animal models support five basic principles regarding a strial form of presbycusis: 1) Progressive EP decline from initially normal levels as a defining characteristic; 2) Non-universality, not all age-associated hearing loss involves EP decline; 3) A clear genetic basis; 4) Modulation by environment or stochastic events; and 5) Independent strial, organ of Corti, and neural pathology. Shared features between human strial presbycusis, gerbils, and BALB/cJ and C57BL/6-Tyr c-2J mice further suggest this condition frequently begins with strial marginal cell dysfunction and loss. By contrast, NOD.NON-H2 nbl mice may model a sequence more closely associated with strial microvascular disease. Additional studies of these and other inbred mouse and rat models should reveal candidate processes and genes that promote EP decline in humans.

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“…12) (Hayashi et al, 2007). Melanocytes throughout the body export melanosomes to the extracellular space, where they may be taken up by neighboring cells (Setaluri, 2000).…”

Section: What Does Cochlear Melanin Protect and When?mentioning

confidence: 99%

“…The protective properties of eumelanin, the principle melanin form in the B6 stria (Bartels et al, 2001;Hayashi et al, 2007), likely derive from its ability to bind cations and transition metals, and to scavenge reactive oxygen species (del Marmol and Beermann, 1996;Riley, 1997;Schraermeyer and Heimann, 1999). Melanin may impact gene transcription or the activity of some enzymes by binding zinc, iron, and copper.…”

Section: Cellular and Molecular Mechanisms Of Melanin's Actionsmentioning

confidence: 99%