The Changes of Na+-K+ ATPase Activity and Ultrastructure of Endolymphatic Secretory Epithelium by Local and Systemic Streptomycin Treatment

Chung, Woon Kyo; Kim, Hee Nam; Lee, Won Sang; Chi, Jang Hoon

Abstract

The endolymphatic secretory epithelium are stria vascularis in cochlear and dark cell in vestibule which are regulated by Na+-K+ ATPase. It is important that we study intracytoplasmic Na+-K+ ATPase for the physiologic research of inner ear. Recently cerium-based method for stain of Na+-K+ ATPase was developed. This study was underkaken to investigate the morphologic changes and Na+-K+ ATPase activity in stria vascularis and vestibular dark cell of mongolian gerbil after systemic intramuscular injection(200mg/kg or 300mg/kg) for 7days or local infiltration of streptomycin through round window. The results are as follows. 1) The strong Na+-K+ ATPase activity was seen at basolateral infoldings of marginal cell in stria vascularis but weak Na+-K+ ATPase activity in dark cell near transitional area. 2) There was no change of Na+-K+ ATPase activity in the stria vascularis and dark cell by systemic injection of streptomycin. The decrease of Na+-K+ ATPase activity in stria vascularis was seen at destruction site of infoldings by local infiltration of streptomycin but no changes in dark cell. 3) The ultrastructural changes of marginal cell by local infiltration of streptomycin were intracytoplasmic vacuole, partial loss of cytoplasmic infoldings, edema, and increase of melanin particle. but, there was no change of ultrastructure in dark cell except increase of melanin particle. The changes of ultrastructure of stria vascularis was variable by systemic streptomycin injection and there was no dark cell change except increased melanin particle. From the above results, the changes of ultrastructure and Na+-K+ ATPase were more severe by local infiltration of streptomycin through round window than systemic injection of streptomycin. The local infiltration of streptomycin through round window may be suitable method for the induction of inner ear damage.