Anatomic and morphometric changes to gerbil posterior cristas following transtympanic administration of gentamicin and streptomycin

• Published in: Journal of the Association for Research in Otolaryngology Vol. 2; no. 2; pp. 147 - 158
• Main Authors: Polgar, R, Collison, T, Slepecky, N B, Wanamaker, H H
• Format: Journal Article
• Language: English
• Published: United States Springer-Verlag 01.06.2001
• Subjects: Animals; Gentamicins - administration & dosage; Gentamicins - poisoning; Gerbillinae; Injections; Semicircular Canals - drug effects; Semicircular Canals - pathology; Streptomycin - administration & dosage; Streptomycin - poisoning; Tympanic Membrane
• ISSN: 1525-3961; 1438-7573
• DOI: 10.1007/s101620010063

Many studies have sought to document ototoxic damage and to study repair and regeneration of mammalian vestibular sensory epithelia. However, linear density analysis of the sensory cells or use of methods that focus on detection of actin in the stereocilia and cuticular plates at the reticular lamina detect only the disappearance of "hair cells" as defined by a narrow set of criteria. The research presented here focuses on the effects of two ototoxic drugs (gentamicin and streptomycin). We used light microscopic analysis of semithin sections to observe changes in the distribution of sensory and supporting cell nuclei and to elucidate other, previously undetected, morphological changes that occurred within the vestibular epithelia. Age-matched untreated and vehicle-treated controls showed that the gerbil posterior crista is asymmetrical on either side of the septum cruciatum; the longer end is taller and narrower than the shorter end. In cross sections taken throughout the length of each posterior crista, the thickness of the sensory epithelium along the sides (peripheral zone) is greater than at the apex (central zone). In tissue sections of the sensory epithelium, the ratio of sensory cell nuclei to support cell nuclei is slightly over 1:1.5 in all regions except the septum cruciatum where most sensory cells are absent and supporting cells predominate. In tissue sections from the most damaged drug-treated specimens, there was a decrease in the linear density of nuclei in the sensory cell layer, with a compensatory increase in the linear density of nuclei in the support cell layer of the sensory epithelia. In these specimens, linear density of total nuclei/tissue section remained the same. In these regions, the width of the epithelium became up to 50% thinner. The ratio of sensory to supporting cell nuclei changed to 1:6. Drug exposure led additionally to a decrease in length of the cristas, but there was not a linear relationship between the change in length of the crista and length of the septum cruciatum in these shorter cristas. In drug-treated cristas, other changes included a decrease in calculated surface area and volume of the epithelia. Thus, while linear density measurements of sensory cell nuclei provide an indication of damage, there are additional anatomic changes to the cristas and caution is advised with regard to interpreting changes as "loss" of cells.