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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Pathological changes in mice with long term cuprizone administration
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Pathological changes in mice with long term cuprizone administration

机译：长期铜沸酮给药小鼠病理变化

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摘要

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). In MS, a long disease duration is known to be a strong risk factor for converting the clinical course of the disease from relapse remitting MS to secondary progressing MS. There is a hypothesis that long sustained demyelination may exhaust neurons, however, pathological changes induced in neurons following demyelination remain unknown. Cuprizone administration can induce and sustain demyelination in the mouse CNS. We examined pathological changes in mice following long sustained demyelination caused by up to 34-week cuprizone administration. Twelve-week cuprizone administration induced severe demyelination in the cerebral cortex, corpus callosum and deep cerebellar nuclei. Demyelination persisted up to 34 weeks, as shown by myelin basic protein immunohistochemistry. In contrast, cuprizone administration developed demyelination in the striatum by week 34. In these demyelinated regions, no neuronal loss was observed. However, in the striatum and deep cerebellar nuclei, cuprizone-induced demyelination changed the intracellular distribution of parvalbumin (PV). Furthermore, in the striatum, there was an increase in PV in the demyelinated axons and most PV immunoreactivity did not co-localize with SMI32 immunoreactivity in mice with 34-week cuprizone administration. Further, mice with 34-week cuprizone administration showed motor coordination dysfunction in the balance beam test. However, 12-week withdrawal from the cuprizone diet induced remyelination in the regions and motor coordination dysfunction recovered. These results indicate that 34-week cuprizone administration induces and sustains demyelination and results in reversible motor coordination dysfunction. The change of intracellular PV distribution suggests that PV may protect demyelinated axons by Ca2+ buffering. This model may be useful to investigate pathological and behavioral changes following demyelination in the CNS.
机译：多发性硬化症（MS）是中枢神经系统（CNS）的炎症脱髓鞘疾病。在MS中，已知长期疾病持续时间是将疾病的临床过程从复发延续的MS转换为二次进展MS的强烈危险因素。有一个假设，即长持续的脱髓鞘可能排气神经元，然而，在脱髓鞘后神经元中诱导的病理变化仍然未知。铜沸酮酮可以在小鼠CNS中诱导和维持脱髓鞘。我们在长期持续脱髓鞘后检查了小鼠的病理变化，冠军长达34周的铜酮酮给药。十二个星期的铜沸酮类诱导脑皮质，胼callosum和深脑核中的严重脱髓鞘。脱髓鞘持续到34周，如髓鞘碱性免疫组织化学所示。相比之下，富沸酮给药在第34周的第34周，在纹状体中发育脱髓鞘。在这些脱髓鞘区域中，没有观察到神经元损失。然而，在纹状体和深脑核中，富沸酮诱导的脱髓鞘改变了帕瓦尔白蛋白（PV）的细胞内分布。此外，在纹状体中，脱髓鞘轴突中的PV增加，大多数光伏免疫反应性在小鼠中没有与34周的小鼠中的小鼠中的SMI32免疫反应性共定位。此外，具有34周的铜沸酮给药的小鼠在平衡梁试验中显示出电动机协调功能障碍。然而，从Cuprizone饮食引起的12周退出诱导的区域和回收的电机协调功能障碍。这些结果表明，34周的铜沸酮给药诱导和维持脱髓鞘并导致可逆电动机协调功能障碍。细胞内PV分布的变化表明PV可以通过CA2 +缓冲保护脱髓鞘轴突。该模型可用于研究CNS中脱髓鞘后的病理和行为变化。

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