[The role of cochlear neurotransmitters in tinnitus]

Abstract

Pathologic changes in the cochlear neurotransmission, e.g. as a result of intensive noise exposure or ototoxic drugs, can be a factor in the development of tinnitus. The efficiency of inhibitory and excitatory neurotransmitters may then be modulated at the switching points. Glutamate is the most important afferent neurotransmitter within the inner ear. A massive glutamate release induced by cochlear damage may result in excitotoxicity and irrevocable cell death. Efferent cochlear neurotransmitters include dopamine, gamma aminobutyric acid (GABA), acetylcholine (ACH) and serotonin. Dopamine and GABA are inhibitory transmitters that may protect the cochlea from excitotoxicity. ACH, like GABA, reduces the stiffness of the outer hair cells and increases their motility. Serotonin is a neuromodulator of the cholinergic and GABAergic innervation within the cochlea and can inhibit glutamatergic impulses. Our understanding of neurotransmission in the cochlea has been extended by advances in molecular biology, which has given rise to new approaches in the treatment of tinnitus. As there are several types of tinnitus, differing in aetiology and development, our present challenge is to achieve precise identification of the cause in individual cases of tinnitus.