The CBA mouse shows little evidence of hearing loss until late in life, whereas the C57BL/6 strain develops a severe and progressive, high-frequency sensorineural hearing loss beginning around 3-6 months of age. These functional differences have been linked to genetic differences in the amount of hair cell loss as a function of age; however, a precise quantitative description of the sensory cell loss is unavailable. The present study provides mean values of inner hair cell (IHC) and outer hair cell (OHC) loss for CBA and C57BL/6 mice at 1, 3, 8, 18, and 26 months of age. CBA mice showed little evidence of hair cell loss until 18 months of age. At 26 months of age, OHC losses in the apex and base of the cochlea were approximately 65% and 50%, respectively, and IHC losses were approximately 25% and 35%. By contrast, C57BL/6 mice showed approximately a 75% OHC and a 55% IHC loss in the base of the cochlea at 3 months of age. OHC and IHC losses increased rapidly with age along a base-to-apex gradient. By 26 months of age, more than 80% of the OHCs were missing throughout the entire cochlea; however, IHC losses ranged from 100% near the base of the cochlea to approximately 20% in the apex.
The inner ear sometimes acts as a robust sound generator, continuously broadcasting sounds (spontaneous otoacoustic emissions) which can be intense enough to be heard by other individuals standing nearby. Paradoxically, most individuals are unaware of the sounds generated within their ears. Two hypotheses could explain this paradox: (1) the spontaneous emissions may not be transmitted to the central nervous system; or (2) the spontaneous emission produces a continuous, high rate of neural activity, which, like the natural pattern of spontaneous activity, is ignored by the central nervous system. Here we demonstrate that high-intensity spontaneous otoacoustic emission can vigorously activate auditory nerve fibres in mammals (Chinchilla laniger). This 'internal biological noise' creates a 'line busy' signal that significantly degrades a neuron's ability to respond to sound and results in a hearing loss completely different from that caused by damage to sensory cells.
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