An animal experimental model of auditory neuropathy induced in rats by auditory nerve compression
An animal experimental model of auditory neuropathy induced in rats by auditory nerve compression
复制标题
听神经压迫致大鼠听神经病变动物实验模型
DOI：
10.1016/j.expneurol.2007.11.006
复制
发表时间：
2008
影响因子：
5.3
通讯作者：
J. Ito
中科院分区：
文献类型：
--
作者：
Masahiro Matsumoto;T. Sekiya;K. Kojima;J. Ito
通过选择性地损伤听神经元或毛细胞，已经建立了几种听神经病（AN）动物模型。药理学病变的特异性通常通过观察可见的结构损伤来评估，但难以定位递送，这可能导致其他解剖结构中的功能副作用。虽然人类AN患者的遗传分析提供了重要的信息AN的病理生理学，特定的遗传缺陷并没有完全相关的听觉神经系统的功能缺陷。为了解决这个问题，我们压缩大鼠听觉神经，以评估长达35周的神经变性。该方法产生了良好的听神经病模型，包括听觉脑干反应的严重恶化和耳蜗微音和畸变产物耳声发射的保留。组织学检查显示，尽管听神经的深度变性，毛细胞保持完整。该模型提供了一个补充替代的基础上的药理学病变和遗传分析的AN患者，并应允许分析的听神经病的病理生理学的风险较小的结果被混淆的未知缺陷，在其他细胞类型。
Several animal models of auditory neuropathy (AN) have been produced by employing pharmacological agents to damage auditory neurons or hair cells selectively. The specificity of pharmacological lesions is generally assessed by observation of visible structural damage but it is difficult to localize the delivery, which could lead to functional side effects in other anatomical structures. Although genetic analyses of human AN patients have provided important information on the pathophysiology of AN, specific genetic defects have not been fully correlated with functional deficits in the auditory nervous system. To address this problem, we compressed rat auditory nerves to assess neural degeneration for up to 35 weeks. The method produced a good model of auditory neuropathy, including profound deterioration of the auditory brainstem response and preservation of both cochlear microphonics and distortion product otoacoustic emissions. Histological examination revealed that in spite of profound degeneration of the auditory nerve, the hair cells remained intact. The model provides a complementary alternative to those based on pharmacological lesions and genetic analyses of AN patients and should allow analysis of the pathophysiology of auditory neuropathy with less risk of the results being confounded by unknown deficits in other cell types.
影响因子：
3.8
作者：
Fleming, JC;Steinkamp, MP;Neufeld, EJ
通讯作者：
Neufeld, EJ
DOI：
10.1016/0168-5597(86)90015-8
发表时间：
1986-09-01
期刊：
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY
影响因子：
--
作者：
MOLLER, AR;BURGESS, J
通讯作者：
BURGESS, J
影响因子：
--
作者：
LEE, MK;TUTTLE, JB;FRANKFURTER, A
通讯作者：
FRANKFURTER, A