Auditory Neural Plasticity in Tinnitus Mechanisms and Management

Figure 2

Possible therapeutic mechanism of glutamate antagonists on salicylate-induced tinnitus. (a) Schematic diagram of the organ of Corti. (b) Salicylate can inhibit the electromotility of OHCs, which reduces the opening probability of MET channels, downregulates the influx of K⁺ through the MET channels, and increases the EP. The sets of three down and three up arrows represent the longitudinal extension of electromotility in OHCs. (c) The increased EP is followed by opening of the voltage-gated Ca²⁺ channels, fusion of the synaptic ribbon to the cytomembrane of the IHCs, and release of glutamate, and thus cochlear fibers depolarize abnormally and tinnitus occurs. Glutamate antagonists can inhibit the process by blocking AMPARs and NMDA receptors. IHC: inner hair cell; OHC: outer hair cell; EP: endocochlear potential; MET: mechanoelectrical transduction; NMDA receptor: N-methyl-D-aspartic acid receptor; AMPAR: α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid receptor.

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