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Furthermore, noise-induced tinnitus models suggest that compensatory mechanisms, potentially involving nitric oxide (NO) signaling, act to increase neuronal gain in the ventral cochlear nucleus in response to reduced input, a process that appears to involve NMDA receptor facilitation (Hockley et al., 2020)

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This interaction produces a hydroxylated 2-pyridine metabolite that effectively inhibits xanthine oxidase, a critical enzyme in uric acid metabolism