Tinnitus is a phantom auditory perception characterized by a ringing sound in either one or both ears. It is a common disorder most often associated with hearing loss and can have a severe impact on a person's quality of life. There is currently no cure and no efficient therapeutic options. There is little known about the neural mechanisms underlying the generation of tinnitus but a better understanding of its neural basis could greatly benefit the development of efficient treatment methods. This literature study aims to explore the neural mechanisms of tinnitus in terms of generation, perpetuation, and perception. Cochlear dysfunction, changes in neuronal firing rates and oscillatory properties, hyperactivity, lack of inhibitory activity and plasticity in auditory-limbic structures have been associated with tinnitus and may be a part of a crossmodal network involved in generating, perpetuating and perceiving tinnitus, through maladaptive CNS plasticity. New developing treatment methods aim to modulate and re-route tinnitus-related plasticity, however, this leads to treatment difficulties due to the crossmodal nature of the tinnitus pathophysiology. These difficulties will be further examined in the discussion.

La polyradiculonévrite inflammatoire démyélinisante chronique (PIDC) est une pathologie neurologique auto-immune du système nerveux périphérique dont la physiopathologie est actuellement mal connue, pour laquelle les options thérapeutiques sont peu nombreuses et dont il n’existe pas de modèle animal fiable. Le premier objectif de ce travail était de valider et de caractériser un modèle animal de PIDC par immunisation de rat Lewis avec le peptide P0(180-199) palmitoylé. Les animaux ont développé une pathologie chronique ou à rechute qui a pu être caractérisée aux plans clinique, histologique, électrophysiologique et immunologique. Les résultats sont en faveur d’un modèle fiable et reproductible mimant bien la PIDC humaine. Le deuxième objectif de ce travail était de tester, sur notre modèle, le fingolimod, modulateur des récepteurs à la sphingosine 1-phosphate, comme potentiel traitement de la pathologie. Le fingolimod a permis, dans notre modèle, de diminuer la sévérité et la chronicité de la maladie, d’améliorer les paramètres électrophysiologiques, de diminuer l’infiltration par les cellules inflammatoires et les anomalies immunologiques. / Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune pathology of the peripheral nervous system whose pathophysiology is currently poorly understood, for which there are few therapeutic options and no reliable animal model. The first aim of this work was to validate and characterize an animal model of CIDP by immunization of rat Lewis with the palmitoylated peptide P0(180-199). The animals developed a chronic or relapsing pathology that could be characterized clinically, histologically, electrophysiologically and immunologically. The results are in favor of a reliable and reproducible model that mimics the human CIDP. The second aim of this work was to test, on our model, the fingolimod, sphingosine 1-phosphate receptor modulator, as potential treatment of the pathology. In our model, fingolimod has reduced the severity and the chronicity of the disease, improved electrophysiological parameters, reduced infiltration by inflammatory cells and recue immunological abnormalities.