Acoustic trauma causes numerous distortions in hearing such as poor frequency resolution, tinnitus, abnormal temporal processing, loudness recruitment and poor speech discrimination. The range of hearing disorders suggests that the underlying pattern of neural is altered significantly. The goal of this project is document the changes that occur in the discharge patterns of single units in the auditory periphery during noise-induced hearing loss and to relate these changes to the audiological disorders and underlying cochlear pathologies. This project has four separate, but related goals: (1) Recent studies suggest that the breakdown in auditory temporal summation may be partially due to changes in the central auditory pathway. One possibility is that acoustic trauma may alter the properties of certain cells in the cochlear nucleus that are known to exhibit temporal summation. Thus, a goal of the project is to determine if acoustic trauma alters the temporal response characteristics of these cells. (2) Listeners with permanent hearing loss often have prolonged forward masking functions. One underlying neural mechanism for this may be a prolongation in the recovery from short-term neural adaptation. This issue will be examined by measuring the time-course of recovery from short-term adaptation in auditory nerve fibers from animals with noise-induced permanent threshold shift. (3) Hearing-impaired listeners also show a reduced ability to detect the sinusoidal amplitude fluctuations in noise. To investigate the underlying neural basis for this temporal resolution, the response patterns of single auditory nerve fibers to sinusoidally amplitude modulated noise will be compared in normal and hearing-impaired listeners. (4) Finally, the loss of tuning, two-tone suppression and lateral inhibition that occurs in single neurons from noise-exposed ears could significantly alter their input/output functions to broadband signals. Therefore, we plan to use broadband noise and determine how acoustic trauma alters the discharge rate-intensity functions of units in the auditory nerve and cochlear nucleus. Ultimately, we will attempt to relate the neural firing patterns seen in units from noise-exposed animals to the underlying cochlear histopathologies as well as to the psychophysical changes that occur in the noise-exposed animals. These results should help to establish a clearer understanding of the anatomical and physiological basis of the audiological symptoms of noise-induced hearing loss. This may potentially lead to better management and treatment of the hearing-impaired listener.
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