Abstract
To study the mechanisms of noise-induced hearing loss and the phantom noise, or tinnitus, often associated with it, we used a mouse model of noise damage designed for reproducible and quantitative structural analyses. We selected the posteroventral cochlear nucleus, which has shown considerable plasticity in past studies, and correlated its changes with the distribution of neurotrophin 3 (NT3). We used volume change, optical density analysis, and microscopic cluster analysis to measure the degeneration after noise exposure. There was a fluctuation pattern in the reorganization of nerve terminals. The data suggest that the source and size of the nerve terminals affect their capacity for regeneration. We hypothesize that the deafferentation of ventral cochlear nucleus is the structural basis of noise-induced tinnitus. In addition, the immunofluorescent data show a possible connection between NT3 and astrocytes. There appears to be a compensatory process in the supporting glial cells during this degeneration. Glia may play a role in the mechanisms of noise-induced hearing loss.