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Viral-mediated Ntf3 overexpression disrupts innervation and hearing in nondeafened guinea pig cochleae

机译:病毒介导的Ntf3过度表达破坏了未聋的豚鼠耳蜗的神经支配和听力

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Synaptopathy in the cochlea occurs when the connection between inner hair cells and the auditory nerve is disrupted, leading to impaired hearing and nerve degeneration. Experiments using transgenic mice have shown that overexpression of NT3 by supporting cells repairs synaptopathy caused by overstimulation. To accomplish such therapy in the clinical setting, it would be necessary to activate the neurotrophin receptor on auditory neurons by other means. Here we test the outcome of NT3 overexpression using viral-mediated gene transfer into the perilymph versus the endolymph of the normal guinea pig cochlea.
机译:当内部毛细胞与听觉神经之间的连接中断时,会发生耳蜗突触病,从而导致听力受损和神经变性。使用转基因小鼠的实验表明,NT3通过支持细胞的过度表达修复了过度刺激引起的突触病。为了在临床环境中完成这种治疗,有必要通过其他方式激活听觉神经元上的神经营养蛋白受体。在这里,我们测试了病毒介导的基因转移到正常豚鼠耳蜗的内淋巴与内淋巴相比,NT3过表达的结果。

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