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Abstract: Tinnitus is one of the most common clinical symptoms of otology, and its pathogenesis is still unclear. The mechanism of tinnitus has been studied through a cognitive progress from the periphery (cochlea) to auditory center to the limbic system. Auditory peripheral lesions, such as damages to ribbon synapses, may form excitatory deafferentation, then it induces the auditory center to start the compensatory gain, leading to an increase in excitatory response; If the damage is further aggravated, it may cause continuous enhancement of central gain effect, hyperexcitability may occur and leading to tinnitus. Besides, the limbic system may be involved in the maintenance or exacerbation of tinnitus symptoms. This paper reviews the recent researches on tinnitus mechanism and auditory center plasticity.
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Key words:
- tinnitus /
- auditory center /
- hyperexcitability /
- ribbon synapse /
- neural plasticity
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