Hair Cell Loss and Synaptic Loss in Inferior Colliculus of C57BL/6 MICE

Spongr, Vlasta P.; Walton, Joseph P.; Frisina, Robert D.; Kazee, Ann Marie; Flood, Dorothy G.; Salvi, Richard

doi:10.1007/978-1-4419-8712-9_49

Cited by 4 publications

(4 citation statements)

References 23 publications

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“…The above results have shown a well-defined hearing phenotype among the four mouse strains kept under the same environmental conditions. The level of hearing loss was found to be most severe for C57BL/6NTac and C57BL/6J, less so for C57BL/6NTac Cdh23+ and absent in C3H/HeJ, which like CBA mice show a very slow decline in their hearing thresholds with age (Spongr et al 1997;Sha et al 2008;Ohlemiller et al 2010). Although the 6N-Repaired strain has an overall better hearing sensitivity than the isogenic 6N mice (Figs 1 and 2), the correction of the hypomorphic allele Cdh23 ahl (Mianné et al 2016) had only a significant impact on frequencies at or above 12 kHz (Fig.…”

Section: Degree Of Hearing Loss In Different Mouse Strainsmentioning

confidence: 90%

Pathophysiological changes in inner hair cell ribbon synapses in the ageing mammalian cochlea

Jeng

Ceriani

Olt

et al. 2020

The Journal of Physiology

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Age-related hearing loss (ARHL) is associated with the loss of inner hair cell (IHC) ribbon synapses, lower hearing sensitivity and decreased ability to understand speech, especially in a noisy environment. r Little is known about the age-related physiological and morphological changes that occur at ribbon synapses. r We show that the differing degrees of ARHL in four selected mouse stains is correlated with the loss of ribbon synapses, being most severe for the strains C57BL/6NTac and C57BL/6J, less so for C57BL/6NTac Cdh23+-Repaired and lowest for C3H/HeJ. r Despite the loss of ribbon synapses with age, the volume of the remaining ribbons increased and the size and kinetics of Ca 2+-dependent exocytosis in IHCs was unaffected, indicating the presence of a previously unknown degree of functional compensation at ribbon synapses. r Although the age-related morphological changes at IHC ribbon synapses contribute to the different progression of ARHL, without the observed functional compensation hearing loss could be greater.

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Section: Degree Of Hearing Loss In Different Mouse Strainsmentioning

confidence: 90%

Pathophysiological changes in inner hair cell ribbon synapses in the ageing mammalian cochlea

Jeng

Ceriani

Olt

et al. 2020

The Journal of Physiology

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“…11,12 Experiments from other investigative teams built on the studies by Willott and coworkers using the C57 strain. For instance, Kazee and coworkers 13 and Sponger and coworkers 14 demonstrated that the number and size of synapses on principal neurons of the auditory midbrain are reduced in C57 mice, but Kazee and West demonstrated that this did not occur in CBA mice of comparable old age. 15 In an immunocytochemical investigation, O'Neill and colleagues 16 discovered that calbindin immunoreactivity in the C57 medial nucleus of the trapezoid body (MNTB) showed a statistically significant decline with age, whereas no reduction was seen in the CBA strain.…”

Section: Conceptual Frameworkmentioning

confidence: 99%

Possible Neurochemical and Neuroanatomical Bases of Age-Related Hearing Loss-Presbycusis

Frisina¹

2001

Semin Hear

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Broadly speaking, age-related hearing loss is a consequence of degenerative changes in the ear or brain. Sensitivity changes in the cochlea result from the loss of sensory (hair) cells, degeneration of auditory nerve fibers (eighth cranial nerve), or reductions in the endocochlear potential resulting from atrophy of the stria vascularis and its biochemical processes normally responsible for production of endolymph. These peripheral problems residing in the inner ear are the primary causes for declines in hearing sensitivity, as reflected in the presbycusic audiogram. The other main presenting symptom for elderly listeners is an inability to perceive speech or music in the presence of background noise. This significant handicap of our aged population, in fact the number one communication deficit of our senior generation, is due not only to losses of peripheral sensitivity to sound but also to age-related neural degeneration of the central auditory system. This article gives summary highlights of recent research on uncovering the neural bases of inner ear disorders and pathologies of the central auditory system that accompany normal aging. Implications for how audiologists and otolaryngologists may improve clinical diagnoses and offer novel future treatments are pointed out.Learning Outcomes: As a result of this activity, the reader will be able to describe new developments in neurochemical and neuroanatomical influences on hearing in older adults.

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“…[33][34][35] The C57BL/6J mouse strain is known for its rapid development of hearing loss with aging. [36][37][38][39] Using C57BL/6J mice that overexpress human XIAP under control of the ubiquitin promoter (ubXIAP), we have found that in comparison with wild-type (WT) littermates, ubXIAP mice showed a delay in the development of presbycusis, which was also associated with a reduction in cochlear HC loss. 40 In this study, we have used these transgenic (TG) mice to determine the effects of XIAP overexpression on NIHL and associated cochlear damage.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of X-linked inhibitor of apoptosis protein protects against noise-induced hearing loss in mice

et al. 2011

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Apoptosis is responsible for cochlear cell death induced by noise. Here, we show that transgenic (TG) mice that overexpress X-linked inhibitor of apoptosis protein (XIAP) under control of the ubiquitin promoter display reduced hearing loss and cochlear damage induced by acoustic overstimulation (125 dB sound pressure level, 6 h) compared with wild-type (WT) littermates. Hearing status was evaluated using the auditory brainstem response (ABR), whereas cochlear damage was assessed by counts of surviving hair cells (HCs) and spiral ganglion neurons (SGNs) as well as their fibers to HCs. Significantly smaller threshold shifts were found for TG mice than WT littermates. Correspondingly, the TG mice also showed a reduced loss of HCs, SGNs and their fibers to HCs. HC loss was limited to the basal end of the cochlea that detects high frequency sound. In contrast, the ABRs demonstrated a loss of hearing sensitivity across the entire frequency range tested (2-32 kHz) indicating that the hearing loss could not be fully attributed to HC loss alone. The TG mice displayed superior hearing sensitivity over this whole range, suggesting that XIAP overexpression reduces noise-induced hearing loss not only by protecting HCs but also other components of the cochlea.

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Hair Cell Loss and Synaptic Loss in Inferior Colliculus of C57BL/6 MICE

Cited by 4 publications

References 23 publications

Pathophysiological changes in inner hair cell ribbon synapses in the ageing mammalian cochlea

Pathophysiological changes in inner hair cell ribbon synapses in the ageing mammalian cochlea

Possible Neurochemical and Neuroanatomical Bases of Age-Related Hearing Loss-Presbycusis

Overexpression of X-linked inhibitor of apoptosis protein protects against noise-induced hearing loss in mice

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