Auditory Threshold Variability in the SAMP8 Mouse Model of Age-Related Hearing Loss: Functional Loss and Phenotypic Change Precede Outer Hair Cell Loss.
KCNQ1 (Kv7.1)
KCNQ4 (Kv7.4)
SAMP8 strain
age-related hearing loss
auditory brainstem response
cytocochleogram
Journal
Frontiers in aging neuroscience
ISSN: 1663-4365
Titre abrégé: Front Aging Neurosci
Pays: Switzerland
ID NLM: 101525824
Informations de publication
Date de publication:
2021
2021
Historique:
received:
11
05
2021
accepted:
09
07
2021
entrez:
19
8
2021
pubmed:
20
8
2021
medline:
20
8
2021
Statut:
epublish
Résumé
Age-related hearing loss (ARHL) is the most common sensory deficit in aging society, which is accompanied by increased speech discrimination difficulties in noisy environments, social isolation, and cognitive decline. The audiometric degree of ARHL is largely correlated with sensory hair cell loss in addition to age-related factors not captured by histopathological analysis of the human cochlea. Previous studies have identified the senescence-accelerated mouse prone strain 8 (SAMP8) as a model for studying ARHL and age-related modifications of the cochlear redox environment. However, the SAMP8 population exhibits a large variability in auditory function decline over age, whose underlying cause remains unknown. In this study, we analyzed auditory function of SAMP8 mice by measuring auditory brainstem response (ABR) thresholds at the age of 6 weeks (juvenile), 12 weeks (young adult), and 24 weeks (adult). Consistent with previous studies, SAMP8 mice exhibit an early progressive, age-related decline of hearing acuity. However, a spatiotemporal cytohistological analysis showed that the significant increase in threshold variability was not concurrently reflected in outer hair cell (OHC) loss observed in the lower and upper quartiles of the ABR threshold distributions over age. This functional loss was found to precede OHC loss suggesting that age-related phenotypic changes may be contributing factors not represented in cytohistological analysis. The expression of potassium channels KCNQ4 (K
Identifiants
pubmed: 34408646
doi: 10.3389/fnagi.2021.708190
pmc: PMC8366269
doi:
Types de publication
Journal Article
Langues
eng
Pagination
708190Informations de copyright
Copyright © 2021 Peixoto Pinheiro, Adel, Knipper, Müller and Löwenheim.
Déclaration de conflit d'intérêts
HL is Scientific Founder and a member of the board of directors of Acousia Therapeutics (Tübingen, Germany). The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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