There is now increasing evidence which suggests that in the absence of impairment in peripheral auditory sensitivity, ge-related changes occur in higher centers of the auditory system. Behavioral studies have demonstrated that speech recognition in elderly listeners is poorer when compared to young listeners matched for hearing sensitivity. Moreover, speech recognition worsens if background noise is added to the speech signal. Unfortunately, little research is available on the neural mechanisms responsible for this age-related deficit. The primary goal of this project is the investigation of neurophysiological correlates which underlie complex sound encoding in quiet and in background noise, in the aged auditory system. Fundamental properties, in frequency and time domains, of complex sound analysis will be studied at the single cell level in the CBA and C57BL/6 strains of mice. These two strains display different age-related hearing dysfunction over their life span, one (CBA) displays a gradual loss in peripheral sensitivity while the other shows rapid auditory dysfunction. Three age-groups of CBAs will be tested, while two of C57BL/6s will be used. Steady state neural coding of sound frequency, as well as dynamic coding of frequency and amplitude modulations will serve as experimental manipulations. More importantly, single neuron responses obtained in quiet will be compared to responses obtained in background noise. In order to rule out age-related peripheral dysfunction which is passed along to more central locations single cell recordings from the inferior colliculus will be compared to responses obtained from auditory nerve fibers, in and across age groups. Finally, the tonotopic organization of the inferior colliculus, in addition , to the afferent neural pathways will be examined using state-of-art methods to quantify age-related changes in neuronal organization.
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