OBJECTIVE: Tinnitus is a phantom auditory sensation, which is mainly triggered by dysfunction of the peripheral auditory organ, such as cochlear disorders. Additionally, the central nervous system, specifically the limbic system, plays a crucial role in the generation and exacerbation of tinnitus. Therefore, to analyze the hypothesis that tinnitus has strong and specific association with the plastic changes in the limbic system, we assessed the neuronal plastic changes in the limbic system, including the hippocampus and the amygdala, in rats with single-sided tinnitus. METHODS: The cochlear damage was achieved by irradiating the cochlea with laser-induced shock wave (LISW). While both hearing loss and tinnitus were confirmed after exposure of rats to LISW, the degree of tinnitus was objectively measured using gap detection behavioral tests. Following the generation of hearing loss and tinnitus, plastic changes in the neurons of the limbic system were confirmed using a molecular marker (activity regulated cytoskeleton-associated protein; Arc). RESULTS: While the expression level of Arc-positive cells in the hippocampal CA1 showed an obvious increase in the hearing loss and tinnitus groups, a significant difference was found between the tinnitus and the control groups. In the dentate gyrus, although the largest number of Arc-positive cells was observed in the tinnitus group, there were no significant differences between the numbers of cells in the hearing loss and tinnitus groups compared to that in the control group. CONCLUSION: Although a significant increase of Arc-positive cells in the hippocampal CA1 was observed between the tinnitus group and control, no obvious tendencies of Arc-positive cells in the limbic system were observed between the rats with and without tinnitus behavior.
