Otoconia and neural junctions of type I hair cells in amikacin-treated guinea pigs presenting saccular acoustic responses.
Using the experimental guinea pig model, in which total and selective destruction of the cochlear receptor revealed saccular acoustic responses, ultrastructural observations were made on otolithic organs using electron microscopy. Scanning electron microscope studies of otoconia from the saccule and utricle of experimental animals did not show any differences with control animals. Quantitative and qualitative observations of sensory neural junctions of Type I cells also did not show any abnormality. These results confirm the extremely selective toxicity of amikacin for the cochlea, and thus strongly suggest that an acoustic reception by the saccule is a normal feature of the guinea pig inner ear.
D000583:Amikacin / Q000633:toxicity*; D000818:Animals; D005072:Evoked Potentials, Auditory; D006168:Guinea Pigs; D006198:Hair Cells, Auditory / Q000648:ultrastructure*; D006199:Hair Cells, Auditory, Inner / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure*; D007612:Kanamycin / Q000031:analogs & derivatives*; D008854:Microscopy, Electron; D008855:Microscopy, Electron, Scanning; D010037:Otolithic Membrane / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure*; D012444:Saccule and Utricle / Q000502:physiology* / Q000648:ultrastructure*; D013569:Synapses / Q000187:drug effects / Q000502:physiology
D007612:Kanamycin; D000583:Amikacin