Age-related hearing impairment in senescence-accelerated mouse (SAM)

Hear Res. 1994 May;75(1-2):27-37. doi: 10.1016/0378-5955(94)90052-3.

Abstract

The auditory brainstem response and histopathology of the cochlea were investigated in an accelerated senescence-prone strain, SAM-P/1 mice and a senescence-resistant strain, SAM-R/1 mice. Each strain displayed an age-related auditory loss expressed as elevated thresholds similar to human hearing loss in that high-frequency losses occurred earlier than middle- or low-frequency losses. SAM-P/1 showed a more rapid decline of hearing with age than did SAM-R/1. Interpeak intervals I-III and I-IV were prolonged with age in both strains, especially at high frequency. The prolongation was more marked in SAM-P/1 than in SAM-R/1. The decrease in amplitude of wave I observed in both strains was greater in SAM-P/1 than in SAM-R/1. The auditory function assessed by thresholds, interpeak intervals and amplitudes of wave I in SAM-P/1 at 12 months of age corresponded roughly to that in SAM-R/1 at 20 months of age. In morphological studies, there was an age-related decrease in the cell density as well as in the size of spiral ganglion neurons in both strains, but these changes were more pronounced in SAM-P/1 than in SAM-R/1. These results reveal that age-related hearing impairment associated with morphological changes in the cochlea is manifested earlier and progresses more rapidly in SAM-P/1 than in SAM-R/1. Thus, the SAM-P/1 strain should prove useful as a model of presbycusis.

Publication types

  • Comparative Study

MeSH terms

  • Aging* / pathology
  • Analysis of Variance
  • Animals
  • Auditory Cortex
  • Auditory Threshold / physiology*
  • Cell Count
  • Cochlea / pathology*
  • Disease Models, Animal
  • Evoked Potentials, Auditory, Brain Stem*
  • Female
  • Male
  • Mice
  • Mice, Inbred Strains
  • Neurons / pathology
  • Presbycusis / pathology
  • Presbycusis / physiopathology*
  • Spiral Ganglion / pathology