Divergence of noise vulnerability in cochleae of young CBA/J and CBA/CaJ mice.

Kevin K Ohlemiller, Mary E Rybak Rice, Erin A Rellinger, Amanda J Ortmann
Author Information
  1. Kevin K Ohlemiller: Program in Audiology and Communication Sciences, Washington University School of Medicine, United States. kohlemiller@wustl.edu

Abstract

CBA/CaJ and CBA/J inbred mouse strains appear relatively resistant to age- and noise-related cochlear pathology, and constitute the predominant 'good hearing' control strains in mouse studies of hearing and deafness. These strains have often been treated as nearly equivalent in their hearing characteristics, and have even been mixed in some studies. Nevertheless, we recently showed that their trajectories with regard to age-associated cochlear pathology diverge after one year of age (Ohlemiller et al., 2010a). We also recently reported that they show quite different susceptibility to cochlear noise injury during the 'sensitive period' of heightened vulnerability to noise common to many models, CBA/J being far more vulnerable than CBA/CaJ (Fernandez et al., 2010 J. Assoc. Res. Otolaryngol. 11:235-244). Here we explore this relation in a side-by-side comparison of the effect of varying noise exposure duration in young (6 week) and older (6 month) CBA/J and CBA/CaJ mice, and in F1 hybrids formed from these. Both the extent of permanent noise-induced threshold shifts (NIPTS) and the probability of a defined NIPTS were determined as exposure to intense broadband noise (4-45 kHz, 110 dB SPL) increased by factors of two from 7 s to 4 h. At 6 months of age the two strains appeared very similar by both measures. At 6 weeks of age, however, both the extent and probability of NIPTS grew much more rapidly with noise duration in CBA/J than in CBA/CaJ. The 'threshold' exposure duration for NIPTS was <1.0 min in CBA/J versus >4.0 min in CBA/CaJ. F1 hybrid mice showed both NIPTS and hair cell loss similar to that in CBA/J. This suggests that dominant-acting alleles at unknown loci distinguish CBA/J from CBA/CaJ. These loci have novel effects on hearing phenotype, as they come into play only during the sensitive period, and may encode factors that demarcate this period. Since the cochlear cells whose fragility defines the early window appear to be hair cells, these loci may principally impact the mechanical or metabolic resiliency of hair cells or the organ of Corti.

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Grants

  1. P30 NS057105/NINDS NIH HHS
  2. P30 DC004665/NIDCD NIH HHS
  3. R01 DC008321/NIDCD NIH HHS
  4. R01 DC003454/NIDCD NIH HHS
  5. T32 DC009975/NIDCD NIH HHS
  6. R01 DC03454/NIDCD NIH HHS

MeSH Term

Acoustic Stimulation
Age Factors
Aging
Analysis of Variance
Animals
Auditory Threshold
Cell Survival
Cochlea
Disease Models, Animal
Evoked Potentials, Auditory, Brain Stem
Female
Genetic Predisposition to Disease
Hair Cells, Auditory
Hearing Loss, Noise-Induced
Male
Mice
Mice, Inbred CBA
Noise
Phenotype
Species Specificity

Word Cloud

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