The spiral ganglion degeneration and the expression of EFR3A in the cochlea of the deaf mice induced by co-administration of kanamycin and furosemide
10.3760/cma.j.issn.1673-0860.2014.11.012
- VernacularTitle:卡那霉素联合呋塞米致聋小鼠耳蜗螺旋神经节细胞的退化变性及其EFR3A蛋白的表达
- Author:
Chen NIE
1
;
Mingliang XIANG
;
Chenling SHEN
;
Haixia HU
;
Bin YE
;
Hao WU
Author Information
1. 200092,上海交通大学医学院附属新华医院耳鼻咽喉头颈外科
- Keywords:
Spiral ganglion;
Nerve degeneration;
Membrane proteins;
Hair cells,auditory;
Mice
- From:
Chinese Journal of Otorhinolaryngology Head and Neck Surgery
2014;49(11):930-936
- CountryChina
- Language:Chinese
-
Abstract:
Objective 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.Methods 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.Results 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.Conclusion 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.
