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首页> 外文期刊>Brain research >Cuprizone effect on myelination, astrogliosis and microglia attraction in the mouse basal ganglia
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Cuprizone effect on myelination, astrogliosis and microglia attraction in the mouse basal ganglia

机译：富沸的效果对小鼠基底神经节在小鼠基础神经节中的髓鞘激华，星分泌症和微胶质增长吸引力

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Multiple sclerosis is the leading cause of neurological disability in young adults affecting more than two million people worldwide. Although multiple sclerosis is generally considered as white matter disease, distinct pathological alterations are also found in the grey matter. Involvement of basal ganglia seems to be related to a set of symptoms such as fatigue, impaired cognition, and movement disturbance. Since no appropriate animal model for studying cortical deep grey matter demyelination is established, we reassessed the cuprizone mouse model to investigate basal ganglia demyelination. Mice were fed cuprizone for different time intervals. The myelin status was analyzed by classical histological staining and immunohistochemistry for myelin proteins and glia markers. Expression of oligodendrocyte and astroglia were investigated by PCR. Cuprizone intoxication induced a severe demyelination of distinct cortical deep grey matter sub-regions. Striosmomes, located within the caudate-putamen and the ventral part of the caudate nucleus displayed intense demyelination, whereas those within the globus pallidus and the head of the caudate nucleus were not affected. The matrix region, however, was equally affected in the medial and lateral region. Besides demyelination, we observed hypertrophic and hyperplastic astrocytosis and microglia cell invasion/local proliferation in the demyelinated areas. Young adult and aged mice were similarly affected as well as mice with different genetic backgrounds. We conclude that cuprizone-induced demyelination provides an adequate animal model to investigate appropriate therapy strategies for the prevention of cortical deep grey matter demyelination. The heterogeneity in local demyelination points at beginning remyelination during ongoing demyelination.
机译：多发性硬化是影响超过200万人的年轻成年人神经病毒残疾的主要原因。虽然多发性硬化通常被认为是白质疾病，但在灰质中也发现了不同的病理改变。基础神经节的参与似乎与一系列症状有关，例如疲劳，认知障碍和运动干扰。由于没有合适的学习皮质深灰色物质脱髓鞘的动物模型，因此我们重新评估了富酮的小鼠模型来调查基​​础神经节脱髓鞘。针对不同的时间间隔喂食铜酮。通过典型的组织学染色和免疫组织化学来分析髓鞘状态，用于髓蛋白和胶质植物标志物。通过PCR研究了脱霉细胞和星形菌细胞的表达。富沸毒性中毒诱导了不同皮质深灰色亚区的严重脱髓鞘。位于凯特 - 腐烂内的尖端和尾部的脊髓孔隙部分显示出强烈的脱髓鞘，而聚菌斑和尾状核的头部不会受到影响。然而，基质区域在内侧和横向区域中同样受到影响。除了脱髓鞘之外，我们还观察到脱髓鞘区域中的肥大和增生星形细胞瘤和微胶质细胞侵袭/局部增殖。年轻成人和年龄的小鼠类似地受到影响以及不同遗传背景的小鼠。我们得出结论，富沸诱导的脱髓鞘提供了足够的动物模型，以研究预防皮质深灰质脱髓鞘的适当治疗策略。在持续脱髓鞘期间在开始重新髓鞘中局部脱髓鞘点的异质性。

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