Acoustic priming and kanamycin-induced chochlear damage.
The cochleae from 3 lines of mice, selectively bred for differential susceptibility to priming-induced audiogenic seizures, were examined following acoustic priming and retest or kanamycin treatment, and the degree of cochlear damage was assessed. After 60 sec of acoustic priming, animals from the high and unselected lines which had subsequently developed audiogenic seizure susceptibility exhibited severe cochlear damage limited to the outer hair cells. Low line mice, which had been selected for resistance to acoustic priming-induced audiogenic seizures and were not seizure susceptible, exhibited no cochlear pathology following acoustic priming. Following kanamycin treatment, all 3 lines developed subsequent audiogenic seizure susceptibility. Histological examination of cochleae from mice so treated revealed a pattern of damage similar to that caused by acoustic priming, except that the cochleae of priming-induced audiogenic seizure resistant low line mice revealed a significant amount of outer hair cell damage. The results are discussed with respect to the physiological mechanism underlying a selectively bred behavioral phenotype in terms of a possible instance of damage/disuse-supersensitivity in the central nervous system.
D000161:Acoustic Stimulation; D000818:Animals; D003051:Cochlea / Q000187:drug effects*; D006198:Hair Cells, Auditory / Q000187:drug effects / Q000648:ultrastructure; D007612:Kanamycin / Q000633:toxicity*; D051379:Mice; D009410:Nerve Degeneration / Q000187:drug effects; D012640:Seizures / Q000139:chemically induced* / Q000235:genetics; D012641:Selection, Genetic
D007612:Kanamycin