| First Author | Saitoh Y | Year | 1994 |
| Journal | Hear Res | Volume | 75 |
| Issue | 1-2 | Pages | 27-37 |
| PubMed ID | 8071152 | Mgi Jnum | J:18564 |
| Mgi Id | MGI:66818 | Doi | 10.1016/0378-5955(94)90052-3 |
| Citation | Saitoh Y, et al. (1994) Age-related hearing impairment in senescence-accelerated mouse (SAM). Hear Res 75(1-2):27-37 |
| abstractText | 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. |
