Abstract
Aminoglycoside ototoxicity is a well-documented process via several pathophysiological pathways. The protective role of cochlear dopamine, released from the lateral olivocochlear efferents, was implicated previously in case of ischemia or acoustic trauma, as it postsynaptically inhibits the effect of excessively released glutamate from the hair cells. In our in vitro superfusion experiments we showed that neomycin dose- dependently inhibits the dopamine release from isolated guinea pig cochlea, while gentamicin and kanamycin was ineffective on it. After chronic application of neomycin the dopamine outflow did not change significantly, suggesting an adaptive process. In our experiments we have found a possibly new action site of one of the aminoglycoside antibiotics, neomycin.
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