The cochlear nucleus (CN) is the first location in the brain where acoustic information from the cochlea is received, processed, and transmitted to other auditory centers. Thus, because the synaptic relationships in the CN play a key role in determining how acoustic information is interpreted by the brain, understanding their anatomy, physiology and biochemistry will advance our comprehension of normal and abnormal hearing. To understand how the CN functions, its cellular and synaptic organization have been studied, and the characteristic electrical responses of its neurons were defined, and are being related to particular types of neurons. Although characteristic reponses are probably important in information processing, an understanding of their basis and how they interact is still limited by the lack of information on the identity and origins of the excitatory and inhibitory inputs to each neuron types. The proposed research attacks this problem by attempting (A), to identify neurons making synapses in the CN that use glutamate, aspartate, glycine, or Gamma-aminobutyric acid as transmitters, and (B), to identify some of the synapses at which these transmitters are used. Experiments will focus on whether axon endings of particular groups of neurons release any of the amino acid transmitters, whether they participate in the inactivation of an amino acid transmitter by high affinity uptake, and whether particular groups of neurons can be identified by transmitter-specific radiolabelling techniques. Surgical interruption of long axonal projections will be used to determine if certain axon endings in the CN are necessary for the electrically evoked release and the high affinity uptake of transmitter candidates. Electron microscopic autoradiographic analysis of uptake sites in unlesioned CN will be used to verify the identification of uptake sites. Transmitter-specific radiolabelling of neurons, visualized by light and electron microscopic autoradiography, will be used to help identify neurons within the CN and projecting to the CN that use particular amino acid transmitters. Since transmitter-specific radiolabelling techniques will label endings and somata of certain neurons, we will probably be in a position in identify the synapses made by several types of neurons and the amino acid transmitter used at those synapses.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
Research Project (R01)
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Communication Sciences and Disorders (CMS)
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University of Connecticut
School of Medicine & Dentistry
United States
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