A substantial number of aged listeners have considerable difficulty in hearing and understanding speech: about half of the people of the United States who are at least 75 years old have this problem, called presbycusis, which seriously impairs communication. The problem is very severe when the listening environment is noisy, with competing sound sources in different locations. Two physiological deficits are responsible for presbycusis. One is a sensory loss in the inner ear; the other is determined by aged related changes in the central auditory system. The former results in a lowered audibility of acoustic input, the second, we hypothesize, results in an inability to follow the rapid fluctuations in amplitude that characterize the speech signal, and to accurate assign them to locations in space. In Project 3 we will search for the neurophysiological correlates of temporal and binaural deficits by characterizing neuronal responses in two key auditory centers, the cochlear nucleus and the inferior colliculus. We will determine whether there are age-related declines in the ability of these neurons to encode temporal signal in noise maskers at different locations. These signals include gaps in noise carriers and sinusoidally modulated tones and noise, presented in control quiet conditions or in background noise. We will examine the possible influence of known age-related changes in the chemical inhibitory systems (GABA and glycine) by examining how antagonists of these neurochemicals might simulate the aged neurons bit in young animals in which these agents are applied to the cells by microiontophoretic techniques; and with Project 4 we investigate the hypothesis that the primary cause of the age-related changes is loss of calcium regulation. The subjects are two models of presbycusis, the C57Bl and the CBA mouse, the first developing a sensory neural loss early in adult life while the second shows little evidence of sensory loss but was shown in our previous work to have substantial losses in temporal processing in later life. The long term objective of this research is to elucidate the physiological basis of presbycusis and its anatomical and neurochemical substrate, with the goal of developing novel and effective treatment modalities for this serious problem.
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