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首页> 外文期刊>Journal of the Association for Research in Otolaryngology: JARO >Ouabain-induced cochlear nerve degeneration: Synaptic loss and plasticity in a mouse model of auditory neuropathy
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Ouabain-induced cochlear nerve degeneration: Synaptic loss and plasticity in a mouse model of auditory neuropathy

机译：哇巴因诱导的耳蜗神经变性：听觉神经病的小鼠模型中的突触损失和可塑性。

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摘要

Ouabain application to the round window can selectively destroy type-I spiral ganglion cells, producing an animal model of auditory neuropathy. To assess the long-term effects of this deafferentation on synaptic organization in the organ of Corti and cochlear nucleus, and to ask whether surviving cochlear neurons show any post-injury plasticity in the adult, we quantified the peripheral and central synapses of type-I neurons at posttreatment times ranging from 1 to 3 months. Measures of normal DPOAEs and greatly reduced auditory brainstem responses (ABRs) confirmed the neuropathy phenotype. Counts of presynaptic ribbons and postsynaptic glutamate receptor patches in the inner hair cell area decreased with post-exposure time, as did counts of cochlear nerve terminals in the cochlear nucleus. Although these counts provided no evidence of new synapse formation via branching from surviving neurons, the regular appearance of ectopic neurons in the inner hair cell area suggested that neurite extension is not uncommon. Correlations between pathophysiology and histopathology showed that ABR thresholds are very insensitive to even massive neural degeneration, whereas the amplitude of ABR wave 1 is a better metric of synaptic degeneration.
机译：将瓦巴因应用于圆窗可选择性破坏I型螺旋神经节细胞，从而产生听觉神经病的动物模型。为了评估这种去除耳聋对Corti和耳蜗核器官中突触组织的长期影响，并询问存活的耳蜗神经元是否在成年人中显示出任何损伤后可塑性，我们量化了I型外周突触和中枢突触后处理时间为1至3个月。正常DPOAEs的测量和大大减少的听觉脑干反应（ABRs）证实了神经病的表型。内毛细胞区域的突触前带和突触后谷氨酸受体斑块的数量随暴露时间的延长而减少，耳蜗核中的耳蜗神经末梢的数量也随暴露时间而减少。尽管这些计数没有提供从存活的神经元分支出新的突触形成的证据，但内毛细胞区域内异位神经元的规则出现表明神经突延伸并不罕见。病理生理学和组织病理学之间的相关性表明，ABR阈值对大规模神经变性都非常不敏感，而ABR波1的振幅是更好的突触变性指标。

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