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- W2095694979 abstract "Gentamicin (GM) has been shown to reversibly reduce the ability of contralateral noise to suppress ipsilateral cochlear activity, in a dose-dependent manner. However, during chronic administration of lower doses (60 mg/kg) the involvement of medial efferents could not be demonstrated. The purposes of the present study were to determine whether other aminoglycosides would display the same acute effects as GM and whether there was any correlation between their specificity and degree of cochlear and vestibular toxicity and their potency of blockade of the medial efferent system.Thus, we observed changes in ipsilateral ensemble background activity (EBA) of the VHIth nerve without and with contralateral low level (55 dB SPL) broadband noise stimulation, in awake guinea pigs (GPs), before and after one single high-dose intramuscular injection of different aminoglycoside antibiotics (AAs) (gentamicin, amikacin, neomycin, netilmicin, streptomycin, tobramycin). For comparison, the effects of strychnine, a known antagonist of the efferent transmission and of cisplatin, an antineoplastic agent with cochleotoxic properties were also studied. Netilmicin displayed blocking properties similar to GM, although less pronounced, while amikacin and neomycin had no effect on medial efferent function. With tobramycin and streptomycin a decrease in suppression was usually associated with a reduction of the EBA measured without acoustic stimulation. However, with cisplatin, suppression was still effective when EBA was severely decreased. We could not observe specific effects of strychnine on medial efferent function. In conclusion, no correlation was found between specificity and degree of AA ototoxicity and their action on the medial efferent system." @default.
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- W2095694979 date "1998-01-01" @default.
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- W2095694979 title "Aminoglycoside Ototoxicity and the Medial Efferent System: II. Comparison of Acute Effects of Different Antibiotics" @default.
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- W2095694979 doi "https://doi.org/10.3109/00206099809072970" @default.
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