螺旋神经节
耳蜗
卡那霉素
医学
耳毒性
速尿
变性(医学)
免疫组织化学
毛细胞
病理
内分泌学
内科学
解剖
生物
化疗
顺铂
基因
生物化学
作者
Chen Nie,Mingliang Xiang,Chenling Shen,Haixia Hu,Bin Ye,Hao Wu
出处
期刊:PubMed
[National Institutes of Health]
日期:2014-11-01
卷期号:49 (11): 930-6
被引量:2
摘要
To investigate the spiral ganglion degeneration and the expression of EFR3A in the cochlea of the deaf mice induced by co-administration of kanamycin and furosemide.Eight weeks old C57BL/6J mice were administered with a single dose of kanamycin followed by furosemide, then fluorescent immunohistochemistry staining and transmission electron microscopy were applied to observe the SGNs' degeneration process and extent characteristics at 1, 5, 15, 30 and 60 days following treatment. We detected the expression of EFR3A during the degeneration of SGNs via fluorescent immunohistochemistry and western blotting.Co-administration of kanamycin and furosemide quickly induced cochlear hair cell death in mice, and then caused progressive degeneration of SGNs. Our results showed that the abnormal morphology of SGNs occurredat day 5 following administration, and the number of SGNs began to decrease at day 15. Compared to the control group, it was found the remarkable increase of the EFR3A protein at the fifth day after co-administration, then decreased to the nearly normal at 15 days following treatment, and no further significant changes thereafter.The changes of the EFR3A protein expression in the spiral ganglion of the cochlea in mice are coincidence with the time of the SGNs degeneration to happen, which imply that EFR3A may play an important role in the occurrence of the SGNs' degeneration in the cochlea in mice following hair cells loss.
科研通智能强力驱动
Strongly Powered by AbleSci AI