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本文引用的文献

1
Survival, synaptogenesis, and regeneration of adult mouse spiral ganglion neurons in vitro.成年小鼠螺旋神经节神经元在体外的存活、突触形成及再生
Dev Neurobiol. 2007 Jan;67(1):108-22. doi: 10.1002/dneu.20336.
2
Free radical scavengers vitamins A, C, and E plus magnesium reduce noise trauma.自由基清除剂维生素A、C和E以及镁可减轻噪声性损伤。
Free Radic Biol Med. 2007 May 1;42(9):1454-63. doi: 10.1016/j.freeradbiomed.2007.02.008. Epub 2007 Feb 20.
3
Mechanisms of noise-induced hearing loss indicate multiple methods of prevention.噪声性听力损失的机制提示了多种预防方法。
Hear Res. 2007 Apr;226(1-2):22-43. doi: 10.1016/j.heares.2006.10.006. Epub 2006 Dec 4.
4
Effects of antioxidants on auditory nerve function and survival in deafened guinea pigs.抗氧化剂对耳聋豚鼠听觉神经功能及存活情况的影响。
Neurobiol Dis. 2007 Feb;25(2):309-18. doi: 10.1016/j.nbd.2006.09.012. Epub 2006 Nov 16.
5
Delayed neurotrophic treatment preserves nerve survival and electrophysiological responsiveness in neomycin-deafened guinea pigs.延迟神经营养治疗可保留新霉素致聋豚鼠的神经存活及电生理反应性。
J Neurosci Res. 2004 Oct 1;78(1):75-86. doi: 10.1002/jnr.20239.
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Caspases, the enemy within, and their role in oxidative stress-induced apoptosis of inner ear sensory cells.胱天蛋白酶——机体内部的敌人及其在氧化应激诱导的内耳感觉细胞凋亡中的作用
Otol Neurotol. 2004 Jul;25(4):627-32. doi: 10.1097/00129492-200407000-00035.
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Localized striatal delivery of GDNF as a treatment for Parkinson disease.局部纹状体递送胶质细胞源性神经营养因子作为帕金森病的一种治疗方法。
Nat Neurosci. 2004 Feb;7(2):105-10. doi: 10.1038/nn1175. Epub 2004 Jan 27.
8
Neurotrophic factors in Huntington's disease.亨廷顿舞蹈症中的神经营养因子
Prog Brain Res. 2004;146:195-229. doi: 10.1016/s0079-6123(03)46014-7.
9
Novel functions and signalling pathways for GDNF.胶质细胞源性神经营养因子的新功能及信号通路
J Cell Sci. 2003 Oct 1;116(Pt 19):3855-62. doi: 10.1242/jcs.00786.
10
BDNF-induced survival of auditory neurons in vivo: Cessation of treatment leads to accelerated loss of survival effects.脑源性神经营养因子在体内诱导听觉神经元存活:停止治疗会导致存活效应加速丧失。
J Neurosci Res. 2003 Mar 15;71(6):785-90. doi: 10.1002/jnr.10542.

胶质细胞系源性神经营养因子和抗氧化剂可在实验性诱导耳聋后保留螺旋神经节神经元的电反应性。

Glial cell line-derived neurotrophic factor and antioxidants preserve the electrical responsiveness of the spiral ganglion neurons after experimentally induced deafness.

作者信息

Maruyama Jun, Miller Josef M, Ulfendahl Mats

机构信息

Center for Hearing and Communication Research, Karolinska Institutet, Sweden.

出版信息

Neurobiol Dis. 2008 Jan;29(1):14-21. doi: 10.1016/j.nbd.2007.07.026. Epub 2007 Aug 11.

DOI:10.1016/j.nbd.2007.07.026
PMID:17870569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2680080/
Abstract

Cochlear implant surgery is currently the therapy of choice for profoundly deaf patients. However, the functionality of cochlear implants depends on the integrity of the auditory spiral ganglion neurons. This study assesses the combined efficacy of two classes of agents found effective in preventing degeneration of the auditory nerve following deafness, neurotrophic factors, and antioxidants. Guinea pigs were deafened and treated for 4 weeks with either local administration of GDNF or a combination of GDNF and systemic injections of the antioxidants ascorbic acid and Trolox. The density of surviving spiral ganglion cells was significantly enhanced and the thresholds for eliciting an electrically evoked brain stem response were significantly reduced in GDNF treated animals compared to deafened-untreated. The addition of antioxidants significantly enhanced the evoked responsiveness over that observed with GDNF alone. The results suggest multiple sites of intervention in the rescue of these cells from deafferentation-induced cell death.

摘要

人工耳蜗植入手术目前是极重度耳聋患者的首选治疗方法。然而,人工耳蜗的功能取决于听觉螺旋神经节神经元的完整性。本研究评估了两类已被发现对预防耳聋后听神经退变有效的药物——神经营养因子和抗氧化剂的联合疗效。将豚鼠致聋,并用局部给予胶质细胞源性神经营养因子(GDNF)或GDNF与抗氧化剂抗坏血酸和生育三烯酚全身注射的组合进行4周治疗。与未治疗的致聋动物相比,接受GDNF治疗的动物中存活的螺旋神经节细胞密度显著增加,诱发电诱发脑干反应的阈值显著降低。添加抗氧化剂后,诱发反应性比单独使用GDNF时显著增强。结果表明,在从去传入诱导的细胞死亡中挽救这些细胞方面存在多个干预位点。