A Longitudinal View of How Noise-Induced Hearing Loss Impacts Auditory and Non- Auditory CNS Activity and the Relationship to Tinnitus Behavior

Abstract

Tinnitus, defined as the perception of sound when no corresponding external sound is present, affects 50 million people in the United States with 2 million reporting decreased quality of life. Although the etiology of tinnitus is heterogeneous, exposure to a damaging auditory stimulus is the most common cause of the perceptual disorder. In addition to the better known auditory component of tinnitus there is an affective component. Anxiety and depression can occur concomitantly with tinnitus and is often of unknown etiology. Exposure to damaging sound leads to complex changes throughout the central nervous system (CNS) impacting both auditory and non-auditory brain areas. The absence of a complete picture of how tinnitus is manifested and maintained in the CNS continues to hinder the development of effective treatments. The goal of this project is to elucidate the underlying mechanisms that produce neuroplastic changes over time in the central nervous system following sound damage that may or may not be associated with tinnitus. Using an animal model of sound induced tinnitus, this project evaluates both early and long-term changes in behavior, neuronal activity, and early changes to neuroplastic protein marker expression in various auditory and non-auditory brain regions. The findings reported here reveal information about the timeline of peripheral injury (sound damage) to tinnitus onset and changes that take place in six different brain regions encompassing both auditory and non-auditory brain regions. This project has allowed us to enhance our understanding of the development of tinnitus over time in several auditory and non-auditory brain structures at both the molecular and systems level in addition to obtaining corresponding changes in behavior.