链霉素耳中毒豚鼠耳蜗外毛细胞外向钾通道的变化  

Changes of K^+ channels of outer hair cells in guinea pig cochlea with streptomycin ototoxicity

作　　者：崔桂英[1] 汤浩[1] 吴玉环[1] 

机构地区：[1]中国医科大学生理学教研室,辽宁沈阳110001

出　　处：《中国病理生理杂志》2002年第6期619-621,共3页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目 (No .394 70 2 4 6 )

摘　　要：目的 :探讨链霉素耳中毒豚鼠耳蜗外毛细胞外向钾通道的变化。方法 :应用听觉脑干诱发电位和全细胞膜片钳制技术。结果 :链霉素耳中毒豚鼠体重明显降低 ;在以 2kHz为主的click刺激时听阈明显升高 ;从链霉素耳中毒豚鼠中分离的外毛细胞数明显减少 ,且以直径较长细胞为主 ;链霉素显著降低豚鼠耳蜗外毛细胞延迟外向K+ 电流 ;链霉素耳中毒豚鼠耳蜗外毛细胞Ca2 + 敏感外向K+ 通道和延迟外向K+ 通道的反转电位与正常对照组相比没有差异。结论 :链霉素对外毛细胞外向钾通道的阻断作用是其耳毒性的基础 ,但不是细胞致死的直接原因。AIM: To study the changes of K + channels of outer hair cells in guinea pig cochlea with streptomycin ototoxicity. METHODS: Auditory brainstem responses (ABR) and whole-cell patch clamp techniques were used.RESULTS: (1) The body weight of guinea pigs with streptomycin ototoxicity decreased significantly; (2) The ABR threshold markedly increased in streptomycin group (Ⅱ,Ⅲ);(3)The number of dissociated outer hair cells of guinea pigs (Ⅱ,Ⅲ) was lower than that of control (Ⅰ); (4) Streptomycin decreased the Ca 2+ -sensitive K + currents and delayed outward K + currents distinctly; (5) There was no significant difference of K + currents between Ⅰ and Ⅱ/Ⅲ. CONCLUSION: These results suggest that the inhibition of K + channels is the basis of streptomycin ototoxicity, but not the direct reason for cell death.

关 键 词：耳中毒 链霉素 耳蜗 钾通道 药物毒性 中毒机制 

分 类 号：R978.12[医药卫生—药品] R961[医药卫生—药学]