Identifying Neural Correlates of Tinnitus: Consequences of Acoustic Trauma on Inferior Colliculus Activity in Unanesthetized Rats

Abstract

Tinnitus, or ringing in the ears, is a condition that affects as many as 50 million Americans. It can be caused by numerous factors, and is considered a symptom rather than a disease. Although it is very prevalent in many susceptible populations, the mechanisms of tinnitus are still not well understood. Most commonly defined as the perception of sound when no corresponding external sound is present, tinnitus was originally thought to be generated in the peripheral auditory system. However, it is currently believed that tinnitus is generated and maintained in central auditory structures. Researchers have spent recent decades seeking to identify the neural correlates of tinnitus in the central auditory system, without much success. Before an effective treatment can be developed for individuals who suffer from tinnitus, it is imperative to understand the underlying mechanisms of the condition. This work summarizes our findings in the context of current tinnitus research. We sought to evaluate changes in spontaneous neural activity in the inferior colliculus of awake, freely moving rats following acoustic trauma. We were able to measure levels of spontaneous activity (SA) following acoustic trauma with the use of both single unit electrophysiology and 14C-2-deoxyglucose assays. By combining these two methods in our animal model of tinnitus, we were not only able to further evaluate SA as a neural correlate of tinnitus, but we were able to address possible problems that tinnitus researchers face, namely the use of anesthesia, varying sound exposure paradigms, and evaluation of both the dominant and non-dominant pathways in the central auditory system.