Our long term goal is to understand the mechanisms that account for the influence of neural activity on synaptic morphology. Neurons of the central auditory pathway and their synaptic connections undergo considerable change as a consequence of deafness, possibly under the direct influence of spike activity in the auditory nerve. Two models of deafness will be investigated in order to study this phenomenon: One model is the acutely deafened cat whose condition can be experimentally-induced- via chemical treatment. The other model is the congenitally deaf white cat, where we know that there is a naturally-occurring progressive loss of sensory receptors with age that begins shortly after birth. This model mimics a heritable hearing disorder found in humans. Significant morphologic changes at the synaptic interface between auditory nerve fibers and cochlear nucleus neurons are observable in both models of deafness. The present proposal seeks to use electrophysiologic and anatomic techniques to examine the role of acute versus chronic hearing loss on the structural integrity of the central auditory system. We will test the hypothesis that auditory nerve activity is an important presynaptic determinant for normal ending structure and postsynaptic neuronal form in the cochlear nucleus. The impact of presynaptic factors on the central auditory pathway across developmental stages will also be studied. Identification of presynaptic variables that affect the central auditory pathway will bear a direct relevance to the processing capabilities of prosthetically restored input. Correlation of the time of onset and form of deafness with these variables may be important in guiding the future selection of promising implant patients.
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