Abstract
Responses of neurons in the central auditory system of ageing mice suggest several sources of age-related problems in hearing. The central representation of frequency (tonotopic organization) is disrupted in mice with presbycusis, implying a cause of problems with frequency coding. In very old mice with only minimal hearing loss, normal-responding neurons co-exist with "sluggish" neurons, which suggests there is a process of attrition that affects some neurons more than others. Spontaneous activity increases in neurons of older mice, implying a decrease in the physiological signal-to-noise ratio. The effects of age-related hearing loss are more severe in the ventral cochlear nucleus than in the dorsal cochlear nucleus, suggesting that various functional circuits may be more or less vulnerable to presbycusis.
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