Kroon Steven, Ramekers Dyan, Smeets Emma M, Hendriksen Ferry G J, Klis Sjaak F L, Versnel Huib
Department of Otorhinolaryngology and Head & Neck Surgery, University Medical Center Utrecht, Room G.02.531, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands.
Department of Otorhinolaryngology and Head & Neck Surgery, University Medical Center Utrecht, Room G.02.531, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands; Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands.
Hear Res. 2017 Mar;345:79-87. doi: 10.1016/j.heares.2017.01.005. Epub 2017 Jan 10.
Damage to and loss of the organ of Corti leads to secondary degeneration of the spiral ganglion cell (SGC) somata of the auditory nerve. Extensively examined in animal models, this degeneration process of SGC somata following deafening is well known. However, degeneration of auditory nerve axons, which conduct auditory information towards the brainstem, and its relation to SGC soma degeneration are largely unknown. The consequences of degeneration of the axons are relevant for cochlear implantation, which is applied to a deafened system but depends on the condition of the auditory nerve. We investigated the time sequence of degeneration of myelinated type I axons in deafened guinea pigs. Auditory nerves in six normal-hearing and twelve deafened animals, two, six and fourteen weeks (for each group four) after deafening were histologically analyzed. We developed a semi-automated method for axon counting, which allowed for a relatively large sample size (20% of the total cross-sectional area of the auditory nerve). We observed a substantial loss of auditory nerve area (29%), reduction in axon number (59%) and decrease in axoplasm area (41%) fourteen weeks after deafening compared to normal-hearing controls. The correlation between axonal degeneration and that of the SGC somata in the same cochleas was high, although axonal structures appeared to persist longer than the somata, suggesting a slower degeneration process. In the first two weeks after induction of deafness, the axonal cross-sectional area decreased but the axon number did not. In conclusion, the data strongly suggest that each surviving SGC possesses an axon.
柯蒂氏器的损伤和丧失会导致听神经螺旋神经节细胞（SGC）胞体的继发性变性。在动物模型中对此进行了广泛研究，耳聋后SGC胞体的这种变性过程是众所周知的。然而，向脑干传导听觉信息的听神经轴突的变性及其与SGC胞体变性的关系在很大程度上尚不清楚。轴突变性的后果与人工耳蜗植入有关，人工耳蜗应用于耳聋系统，但取决于听神经的状况。我们研究了耳聋豚鼠有髓I型轴突变性的时间顺序。对6只听力正常和12只耳聋动物在耳聋后2周、6周和14周（每组4只）的听神经进行了组织学分析。我们开发了一种半自动轴突计数方法，该方法允许进行相对较大的样本量（占听神经总横截面积的20%）。与听力正常的对照组相比，我们观察到耳聋14周后听神经面积大幅减少（29%）、轴突数量减少（59%）和轴浆面积减少（41%）。同一耳蜗中轴突变性与SGC胞体变性之间的相关性很高，尽管轴突结构似乎比胞体持续的时间更长，这表明变性过程较慢。在耳聋诱导后的前两周，轴突横截面积减小，但轴突数量没有减少。总之，数据强烈表明每个存活的SGC都拥有一条轴突。
