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The osmotic demyelination syndrome: the resilience of thalamic neurons is verified with transmission electron microscopy

机译:渗透脱髓鞘综合征:用透射电子显微镜验证丘脑神经元的韧带

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摘要

The development of a murine model of osmotic demyelinating syndrome (ODS) allowed to study changes incurred in extrapontine zones of the CNS and featured neuron and glial cell changes in the relay thalamic ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei before, during and after ODS induction, and characterized without immune response. There, the neuron Wallerian-type deteriorations were verified with fine structure modifications of the neuron cell body, including some nucleus topology and its nucleolus changes. Morphologic analyses showed a transient stoppage of transcriptional activities while myelinated axons in the surrounding neuropil incurred diverse damages, previously reported. Even though the regional thalamus myelin deterioration was clearly recognized with light microscopy 48 h after osmotic recovery of ODS, ultrastructure analyses demonstrated that, at that time, the same damaged parenchyma regions contained nerve cell bodies that have already reactivated nucleus transcriptions and neuroplasm translations because peculiar accumulations of fibro-granular materials, similar to those detected in restored ODS astrocytes, were revealed in these restructuring nerve cell bodies. Their aspects suggested to be accumulations of ribonucleoproteins. The findings suggested that progressive neural function's recovery in the murine model could imitate some aspects of human ODS recovery cases.
机译:渗透性脱髓鞘综合征(ODS)小鼠模型的建立允许研究中枢神经系统脑桥外区发生的变化,以及在ODS诱导之前、期间和之后丘脑腹后外侧(VPL)和腹后内侧(VPM)中继核中神经元和胶质细胞的变化,其特征是无免疫反应。在那里,神经元沃勒氏类型的退化通过神经元胞体的精细结构修改得到证实,包括一些细胞核拓扑结构及其核仁变化。形态学分析显示,转录活动暂时停止,而周围神经纤维中的有髓轴突引起了不同程度的损伤。尽管在ODS渗透恢复48小时后,光学显微镜可以清楚地识别出局部丘脑髓鞘退化,但超微结构分析表明,当时,同样受损的实质区域含有神经细胞体,由于纤维颗粒物质的特殊堆积,这些神经细胞体已经重新激活了细胞核转录和神经质翻译,与在修复的ODS星形胶质细胞中检测到的类似,在这些重组的神经细胞体中也发现了类似的结果。它们的特性表明是核糖核蛋白的积累。研究结果表明,在小鼠模型中进行性神经功能恢复可以模拟人类ODS恢复病例的某些方面。

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