Tinnitus is a pathology, which severely impairs the quality of life, and for which no efficient therapy exists. One reason is the lack for clear understanding of the molecular mechanisms of this pathology. For example, the anatomical site and the molecular pathways responsible for the generation of tinnitus are still under debate. This is due, in part, to the difficulty to induce and measure tinnitus in animals. This paper summarizes the recent discoveries provided by the use of salicylate as a model of tinnitus. The first is the demonstration that salicylate acts at the periphery by activating on cochlear NMDA receptors that are not "normally" implicated in the transmission of auditory message to the brain. The second discovery is the clear demonstration that strong relationships exist between anxiety and perception of tinnitus. Interestingly, application of NMDA antagonists onto the round window membrane abolished tinnitus, even in animals receiving a treatment with the anxiogenic serotonergic agent meta-chlorophenylpiperazine (mCPP). In addition to classical psychotherapeutic treatments, targeting cochlear NMDA receptors, by local infusion of drugs into the middle ear to reach the cochlea, may represent a promising therapeutic strategy to cure incapacitating tinnitus, even in depressed or chronically anxious patients.