This experiment was conducted to investigate the time-dependent effects of gentamicin (GM) on the neuroepithelial morphology of the posterior crista ampullares (PCA) of the adult chinchilla. The time course of GM-induced HC pathology was documented through measurements of HC density as well as through HC morphologic evaluation. HC morphology was examined under light microscopy and HC density measurements were documented as a function of the time course of GM-induced ototoxicity. Six groups of animals (n=12) were treated with daily injections of 30 mg/kg of GM subcutaneously (SC) for six days and were sacrificed 1, 2, 3, 4, 6 and 8 weeks post-treatment. An untreated control group (n=3) was employed. Morphologically, in the first two weeks post-treatment (PT), there was pronounced GM-induced pathology in the crista neuroepithelia (NE), with clear fusion of ciliary bundles, blebs, cytoplasmic vacuolization and shrinkage of the cytoplasm. The NE recovered from the induced pathology at three weeks post-treatment, displaying a normal morphology which remained unchanged up to 8 weeks post-treatment. Quantitatively, there was a significant decrease (p

This experiment was conducted to investigate the time-dependent effects of gentamicin (GM) on the neuroepithelial morphology of the posterior crista ampullares (PCA) of the adult chinchilla. The time course of GM-induced HC pathology was documented through measurements of HC density as well as through HC morphologic evaluation. HC morphology was examined under light microscopy and HC density measurements were documented as a function of the time course of GM-induced ototoxicity. Six groups of animals (n=12) were treated with daily injections of 30 mg/kg of GM subcutaneously (SC) for six days and were sacrificed 1, 2, 3, 4, 6 and 8 weeks post-treatment. An untreated control group (n=3) was employed. Morphologically, in the first two weeks post-treatment (PT), there was pronounced GM-induced pathology in the crista neuroepithelia (NE), with clear fusion of ciliary bundles, blebs, cytoplasmic vacuolization and shrinkage of the cytoplasm. The NE recovered from the induced pathology at three weeks post-treatment, displaying a normal morphology which remained unchanged up to 8 weeks post-treatment. Quantitatively, there was a significant decrease (p