The studies can be divided into two main areas: 1) those intended to elucidate the ways in which the normal patterns of neural activity in the peripheral auditory system are generated, and 2) those intended to understand the mechanisms by which noise exposure can cause temporary and/or permanent hearing deficits. Experiments in both these areas focus on the correlation between structure of the peripheral auditory system (both at the light- and electron-microscopic levels) and the function of the system, as seen in the response of single neurons. The precision of these correlations is greatly enhanced by the application of single-neuron labeling techniques, which allow us to follow single, physiologically identified neurons from their origins to their terminations. The experiments on the normal auditory system are focused on the efferent system. In most vertebrate ears, the sensory cells and/or afferent nerve fibers receive an efferent innervation. This system presumably plays a feedback role in modifying the output of the afferent neurons according to the nature of the acoustic input. We know that electrical stimulation of this efferent system in mammals leads to an increase in the thresholds of afferent neurons. However, we know relatively little of the nature of the sound-evoked activity of single efferent neurons or their cochlear innervation patterns. This type of fundamental information will emerge from the proposed studies of intracellular recording and labeling of single efferent neurons in the cat. The resultant data should form the basis for more realistic speculation about the role of this system in the overall process of auditory perception. The studies on noise-damaged cochleas have two main aims. The first is to infer normal cochlear mechanisms by comparing the changes in auditory-nerve activity with the structural and ultrastructural alterations in the sensory cells which give rise to them. The application of intracellular labeling techniques allow these correlations to be made on the single-cell level. The second main aim is to describe the structural changes underlying permanent vs. temporary threshold shifts and, most importantly, to understand the nature of the acute changes which determine whether the effects of a given exposure will be reversible or irreversible. The combination of physiological and morphological techniques we have in hand put us in a unique position to address this question. If the dynamics of the repair process can be understood, it is possible that post-trauma treatment can be devised to improve the final outcome.
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