Synaptic and transmitter biochemistry and plasticity in the in the auditory parts of the adult brain. Hearing loss, which affects over 28 million people in the U.S.A., is accompanied by additional pathological symptoms, such as tinnitus (phantom sound), misperception of loudness and degraded ability to detect meaningful sounds in a noisy environment. An effective treatment for these symptoms has yet to be established. Since altered synaptic signaling is thought to generate these symptoms, we focus on auditory neural pathways to understand how hearing impairment alters synaptic biochemistry and structure. Biochemical, molecular and immunohistochemical methods (A) identify transmitters, receptors, regulatory and cell signaling pathways, and (B) determine the regulatory and signal transduction mechanisms underlying transmitter, receptor and synaptic plasticities induced by hearing loss. Neuroanatomical methods define altered synaptic organization. We find that in adults, surgical or noise lesions of the cochlea that produce hearing loss reorganize synaptic connections in brain auditory structures. Some of the consequences include synaptic pruning, synaptogenesis, an increased strength of excitatory transmission and deficient inhibitory transmission. These plasticities appear to be driven by signal transduction pathways which alter regulatory mechanisms.

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