Abstract：
Spiral ganglion neurons (SGNs) transmit sound signals received by hair cells to the auditory center to produce hearing. The quantity and function are important for maintaining normal hearing function. Limited by the regenerative capacity, SGNs are unable to regenerate spontaneously after injury. Various neurotrophic factors play an important role in the regeneration process. Neuritin is a neurite growth factor that plays an important role in neural plasticity and nerve injury repair. In this study, we used bioinformatics analysis to show that neuritin was negatively correlated with cochlear damage. Then, we aimed to establish a cochlear spiral ganglion-specific sensorineural deafness model in gerbils using ouabain and determine the effects of exogenous neuritin protein in protecting damaged cochlear SGNs and repairing damaged auditory nerve function. The provides a new research strategy and scientific basis for the prevention and treatment of sensorineural deafness caused by the loss of SGNs. We were discovered that neuritin is expressed throughout the development of the gerbil cochlea, primarily in the SGNs and Corti regions. The expression of neuritin was negatively correlated with the sensorineural deafness induced by ouabain. In vitro and in vivo revealed that neuritin significantly maintained the number and arrangement of SGNs and nerve fibers in the damaged cochlea and effectively protected the high-frequency listening function of gerbils.
摘要：
螺旋神经节神经元（SGN）将毛细胞接收到的声音信号传送到听觉中枢以产生听觉。数量和功能对于维持正常的听力功能很重要。受再生能力的限制，SGN在受伤后不能自发再生。各种神经营养因子在再生过程中起重要作用。Neuritin是一种神经突生长因子，在神经可塑性和神经损伤修复中起重要作用。在这项研究中,我们通过生物信息学分析显示神经素与耳蜗损伤呈负相关。然后，我们的目的是使用哇巴因建立沙鼠耳蜗螺旋神经节特异性感音神经性耳聋模型，并确定外源性神经素蛋白在保护受损的耳蜗SGN和修复受损的听觉神经功能中的作用。为SGNS丢失所致感音神经性耳聋的防治提供了新的研究策略和科学依据。我们发现神经素在沙鼠耳蜗的整个发育过程中都有表达，主要在SGN和Corti地区。神经素的表达与哇巴因诱发的感音神经性耳聋呈负相关。体外和体内实验表明，神经素显著维持了受损耳蜗中SGN和神经纤维的数量和排列，有效保护了沙鼠的高频听音功能。
