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目的:探讨感音神经性聋发生后小鼠耳蜗外侧壁形态和功能的改变。方法:选用3-4周龄的CBA/J小鼠为实验对象,联合应用卡那霉素及呋塞米致聋。在给药后0.5 d、1 d、2 d、7 d、28 d及112 d监测耳蜗内电位(EP)的改变;应用HE染色、免疫化学和透射电镜方法检测耳蜗外侧壁形态以及2种K+转运蛋白NKCC1和α2Na,K-ATPase的变化。结果:序贯应用卡那霉素及呋塞米后0.5 d小鼠EP开始下降,至1 d进行性下降,至2 d完全恢复正常并在随后长时期保持稳定。HE染色显示毛细胞损失和耳蜗外侧壁萎缩是主要病理改变。免疫化学结果表明耳蜗外侧壁NKCC1和α2Na,K-ATPase蛋白表达明显下降。透射电镜结果显示血管纹厚度在致聋后进行性下降,主要为边缘细胞萎缩造成。结论:萎缩后的耳蜗外侧壁在毛细胞严重缺失的情况下仍然可以保证EP的正常维持。
Objective: To investigate the changes of morphology and function of outer cochlear wall of mice after sensorineural deafness. Methods: CBA / J mice of 3-4 weeks old were used as experimental subjects, combined with kanamycin and furosemide-induced deafness. The changes of EP within the cochlea were observed at 0.5 d, 1 d, 2 d, 7 d, 28 d and 112 d after administration. HE staining, immunochemistry and transmission electron microscopy were used to detect the morphology of the cochlear lateral wall and the changes of two K + Changes of transporter NKCC1 and α2Na, K-ATPase. Results: After 0.5 days of sequential application of kanamycin and furosemide, the EP of mice began to decline and gradually decreased to the first day, completely returned to normal after 2 days and remained stable for a long period of time. HE staining showed that hair loss and cochlear lateral wall atrophy were the main pathological changes. Immunochemical results showed that the outer wall of cochlear NKCC1 and α2Na, K-ATPase protein expression decreased significantly. Transmission electron microscopy showed that the thickness of vascular smoothing decreased after deafness, mainly caused by atrophy of marginal cells. CONCLUSIONS: The atrophic cochlear outer wall can still maintain the normal maintenance of EP even in the absence of hair cells.