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首页> 外文期刊>Development >NeuroD-null mice are deaf due to a severe loss of the inner ear sensory neurons during development.
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NeuroD-null mice are deaf due to a severe loss of the inner ear sensory neurons during development.

机译：由于发育期间内耳感觉神经元的严重丧失，NeuroD-null小鼠失聪。

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摘要

A key factor in the genetically programmed development of the nervous system is the death of massive numbers of neurons. Therefore, genetic mechanisms governing cell survival are of fundamental importance to developmental neuroscience. We report that inner ear sensory neurons are dependent on a basic helix-loop-helix transcription factor called NeuroD for survival during differentiation. Mice lacking NeuroD protein exhibit no auditory evoked potentials, reflecting a profound deafness. DiI fiber staining, immunostaining and cell death assays reveal that the deafness is due to the failure of inner ear sensory neuron survival during development. The affected inner ear sensory neurons fail to express neurotrophin receptors, TrkB and TrkC, suggesting that the ability of NeuroD to support neuronal survival may be directly mediated through regulation of responsiveness to the neurotrophins.
机译：神经系统的遗传程序性发育的关键因素是大量神经元的死亡。因此，控制细胞存活的遗传机制对发育神经科学至关重要。我们报告说，内耳感觉神经元依赖于称为NeuroD的基本螺旋-环-螺旋转录因子在分化过程中的存活。缺乏NeuroD蛋白的小鼠没有听觉诱发电位，反映出严重的耳聋。 DiI纤维染色，免疫染色和细胞死亡分析表明，耳聋是由于发育过程中内耳感觉神经元存活失败所致。受影响的内耳感觉神经元无法表达神经营养蛋白受体TrkB和TrkC，这表明NeuroD支持神经元存活的能力可能是通过对神经营养蛋白的反应性调节直接介导的。

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