Dupont J, Guilhaume A, Aran J M
Laboratoire d'Audiologie Expérimentale, INSERM Unité 229 et Université de Bordeaux II, Hôpital Pellegrin, France.
Hear Res. 1993 Aug;68(2):217-28. doi: 10.1016/0378-5955(93)90125-k.
This paper reports on a dynamic study of the morphological changes within the cochlear and vestibular ganglia of the guinea pig after local application of Sisomicin in the inner ear. The treatment leads to a rapid, complete and irreversible destruction of the sensory cells in the cochlear and vestibular neuroepithelia. A progressive degeneration of the type I and type II afferent neurons, presenting a decreasing gradient from the base towards the apex of the cochlea, is rapidly observed and becomes almost complete as early as 15 days after the peripheral injury. Five months after the treatment the spiral ganglion cells have almost completely disappeared. At this time the vestibular ganglion cell density appears normal but the neurons exhibit important signs of alteration. Such damage to the cochlear and vestibular afferent neurons may result from either retrograde neuronal degeneration and/or direct neurotoxic effect of the drug. Thus the combination of the two mechanisms could lead to neuronal losses in spiral and Scarpa's ganglia after the local aminoglycoside intoxication of the inner ear. The difference in the time course of degeneration for these two afferent ganglia could be due to their specific susceptibilities or to their different anatomical locations.
本文报道了在内耳局部应用西索米星后豚鼠耳蜗和前庭神经节形态变化的动态研究。该治疗导致耳蜗和前庭神经上皮中的感觉细胞迅速、完全且不可逆地破坏。I型和II型传入神经元进行性退化,从耳蜗底部到顶部呈递减梯度,在外周损伤后15天就迅速观察到,并且早在此时几乎就已完全退化。治疗五个月后,螺旋神经节细胞几乎完全消失。此时前庭神经节细胞密度看似正常,但神经元呈现出重要的改变迹象。耳蜗和前庭传入神经元的这种损伤可能源于逆行性神经元变性和/或药物的直接神经毒性作用。因此,这两种机制的结合可能导致内耳局部氨基糖苷类中毒后螺旋神经节和斯卡帕神经节中的神经元损失。这两个传入神经节退化时间进程的差异可能是由于它们的特定易感性或不同的解剖位置。