Quantitative evaluation of cochlear neurons and computer-aided three-dimensional reconstruction of spiral ganglion cells in humans with a peripheral loss of nerve fibres

Quantitative evaluation of cochlear neurons and computer-aided three-dimensional reconstruction of spiral ganglion cells in humans with a peripheral loss of nerve fibres
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DOI:
10.1016/s0378-5955(96)00209-2
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发表时间:
1997-03-01
期刊:
影响因子:
2.8
通讯作者:
SchrottFischer, A
SchrottFischer, A
中科院分区:
医学1区
文献类型:
--
作者:
Felder, E;Kanonier, G;SchrottFischer, A

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从5例老年性耳聋患者和2例听力正常患者的不同区域收集了人类耳蜗神经元元素的定量数据。螺旋板和内耳道中的神经纤维的数量与螺旋神经节细胞的计数一起进行评估。结果表明,神经元数量在外周减少,即,随着与中枢神经系统距离的增加,老年性耳聋患者的高音听力损失。在两名听力正常的患者中,与内耳道相比,螺旋板中的神经元数量没有显着差异。人类螺旋神经节的计算机辅助三维重建显示了大的双极神经元(I型细胞),但也有一个缺失轴突的大神经节细胞。结果提示老年性聋从外周到螺旋神经节呈缓慢的退行性变。对新鲜固定的人类螺旋神经节的透射电子显微镜分析显示了神经间连接。据推测,在螺旋神经节水平上来自其他神经元的营养供应是否可以防止或延迟中央轴突的进一步变性。
Quantitative data on human cochlear neuronal elements were collected from various regions in five patients with high-tone hearing loss due to presbycusis and in two patients with normal hearing. The number of nerve fibres was assessed in the spiral lamina and in the inner acoustic meatus together with counts of spiral ganglion cells. The results show that the number of neurons decreased peripherally, i.e., with increasing distance from the central nervous system in patients with high-tone hearing loss due to presbycusis. In two patients with normal hearing no significant difference in the number of neurons was found in the lamina spiralis as compared to the inner acoustic canal. Computer-aided 3-dimensional reconstruction of the human spiral ganglion displayed large bipolar neurons (type I cells), but also large ganglion cells with one missing axon. The results may indicate that a slow retrograde degeneration occurs from the periphery towards the spiral ganglion in presbycusis. Transmission electron microscopy analysis of freshly fixed human spiral ganglions displayed interneural connections. It is speculated whether a trophic supply from other neurons at the level of the spiral ganglion can prevent or delay further degeneration of the central axon.