Molecular Biology of the Central Auditory System and Tinnitus

Tinnitus is an auditory precept without any external input. In most cases, initial damage to the cochlea results in a change in peripheral auditory input that, in turn, triggers a change in central auditory mechanisms to compensate for this loss. This compensation, a combination of homeostatic and synaptic plasticity, results in an increased ‘gain’ in central auditory structures that may underlie the initiation of tinnitus. Changes at the molecular, cellular, and synaptic level in both auditory and nonauditory areas have been noted in animal models of tinnitus. Current research efforts to cure or clinically target to alleviate the tinnitus symptoms are focused on these areas and target these changes, including ion channel activators. Future studies should focus on unraveling the mechanisms of tinnitus precept induction and circuitry distribution for better treatment options.