|Donald M. Caspary, Ph.D.
Professor, Distinguished Scholar
Age-related hearing loss (presbycusis) is a complex state which may reflect pathological influences along the entire auditory system. For certain kinds of age-related hearing loss, there is a dramatic loss of speech understanding without a parallel loss in pure-tone thresholds. This loss is especially severe under noisy conditions. Central auditory dysfunction in aging may be in response to partial peripheral deafferentation and may be similar to changes observed with noise exposure or ototoxic drugs. In many ways, the underlying causes of tinnitus, the hearing of phantom sounds, may also reflect changes due to the partial deafferentation of the central auditory processor. These changes may involve changes in the synthesis, degradation, uptake, release and receptor sensitivity of neurotransmitter systems. Studies in our laboratory are focused on the understanding of two closely related questions in auditory research:
Studies in most central auditory structures have found that inhibitory neurotransmitters are critically involved in coding acoustic information. Coding of these signals appears vulnerable to the aging process and to the peripheral damage frequently observed in tinnitus. Studies of circuits within the central auditory system undergo age-related and tinnitus-related changes to pre and postsynaptic GABAergic and glycinergic neurotransmission. Ongoing projects in the laboratory are focused on how the brain changes its ability to process auditory signals as we age and in animal models of tinnitus. Neurochemical and molecular studies are examining how receptors in auditory structures change their structural makeup with the partial deafferentation seen in aging and tinnitus. We also examine the mechanisms which trigger these receptor changes. A clear understanding of plastic changes within central auditory circuits could lead to the development of pharmacotherapy for tinnitus and for age-related hearing loss.