Spontaneous and Partial Repair of Ribbon Synapse in Cochlear Inner Hair Cells After Ototoxic Withdrawal

被引:23
作者
Liu, Ke [1 ]
Chen, DaiShi [1 ]
Guo, WeiWei [1 ]
Yu, Ning [1 ]
Wang, XiaoYu [1 ]
Ji, Fei [1 ]
Hou, ZhaoHui [1 ]
Yang, Wei-Yan [1 ]
Yang, ShiMing [1 ]
机构
[1] Chinese Peoples Liberat Army Gen Hosp, Inst Otolaryngol, Dept Otolaryngol Head & Neck Surg, Beijing 100853, Peoples R China
基金
北京市自然科学基金; 中国博士后科学基金; 中国国家自然科学基金;
关键词
Sensorineural deafness; Cochlea; Ribbon synapse; Ototoxic exposure; RIBEYE/CtBP2; LONG-TERM FACILITATION; AMINOGLYCOSIDE OTOTOXICITY; GENTAMICIN; MECHANISMS; EXOCYTOSIS; REPLENISHMENT; PERMEABILITY; DEGENERATION; EXPRESSION; OTOFERLIN;
D O I
10.1007/s12035-014-8951-y
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ototoxicity is one of the major causes of sensorineural deafness. However, it remains unclear whether sensorineural deafness is reversible after ototoxic withdrawal. Here, we report that the ribbon synapses between the inner hair cells (IHCs) and spiral ganglion nerve (SGN) fibers can be restored after ototoxic trauma. This corresponds with hearing restoration after ototoxic withdrawal. In this study, adult mice were injected daily with a low dose of gentamicin for 14 consecutive days. Immunostaining for RIBEYE/CtBP2 was used to estimate the number and size of synaptic ribbons in the cochlea. Hearing thresholds were assessed using auditory brainstem responses. Auditory temporal processing between IHCs and SGNs was evaluated by compound action potentials. We found automatic hearing restoration after ototoxicity withdrawal, which corresponded to the number and size recovery of synaptic ribbons, although both hearing and synaptic recovery were not complete. Thus, our study indicates that sensorineural deafness in mice can be reversible after ototoxic withdrawal due to an intrinsic repair of ribbon synapse in the cochlea.
引用
收藏
页码:1680 / 1689
页数:10
相关论文
共 47 条
[1]   The fate of outer hair cells after acoustic or ototoxic insults [J].
Abrashkin, Karen A. ;
Izumikawa, Masahiko ;
Miyazawa, Toru ;
Wang, Chih-Hung ;
Crumling, Mark A. ;
Swiderski, Donald L. ;
Beyer, Lisa A. ;
Gong, Tzy-Wen L. ;
Raphael, Yehoash .
HEARING RESEARCH, 2006, 218 (1-2) :20-29
[2]   Involvement of the mitochondrial permeability transition in gentamicin ototoxicity [J].
Dehne, N ;
Rauen, U ;
de Groot, H ;
Lautermann, J .
HEARING RESEARCH, 2002, 169 (1-2) :47-55
[3]   Mechanisms of rapid sensory hair-cell death following co-administration of gentamicin and ethacrynic acid [J].
Ding, Dalian ;
Jiang, Haiyan ;
Salvi, Richard J. .
HEARING RESEARCH, 2010, 259 (1-2) :16-23
[4]   Leupeptin protects cochlear and vestibular hair cells from gentamicin ototoxicity [J].
Ding, DL ;
Stracher, A ;
Salvi, RJ .
HEARING RESEARCH, 2002, 164 (1-2) :115-126
[5]   Aminoglycoside antibiotics [J].
Forge, A ;
Schacht, J .
AUDIOLOGY AND NEURO-OTOLOGY, 2000, 5 (01) :3-22
[6]   Mechanisms contributing to synaptic Ca2+ signals and their heterogeneity in hair cells [J].
Frank, Thomas ;
Khimich, Darina ;
Neef, Andreas ;
Moser, Tobias .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2009, 106 (11) :4483-4488
[7]   Transmitter release at the hair cell ribbon synapse [J].
Glowatzki, E ;
Fuchs, PA .
NATURE NEUROSCIENCE, 2002, 5 (02) :147-154
[8]   Ototoxic Effects of Single-Dose versus 19-Day Daily-Dose Gentamicin [J].
Gooi, Adrian ;
Hochman, Jordan ;
Wellman, Mark ;
Blakley, Laura ;
Blakley, Brian W. .
JOURNAL OF OTOLARYNGOLOGY-HEAD & NECK SURGERY, 2008, 37 (05) :664-667
[9]   Fast vesicle replenishment allows indefatigable signalling at the first auditory synapse [J].
Griesinger, CB ;
Richards, CD ;
Ashmore, JF .
NATURE, 2005, 435 (7039) :212-215
[10]   Gentamicin induced nitric oxide-related oxidative damages on vestibular afferents in the guinea pig [J].
Hong, SH ;
Park, SK ;
Cho, YS ;
Lee, HS ;
Kim, KR ;
Kim, MG ;
Chung, WH .
HEARING RESEARCH, 2006, 211 (1-2) :46-53