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| 1 | Clemastine rescues behavioral changes and enhances remyelination in the cuprizone mouse model of demyelination显示文摘Increasing evidence suggests that white matter disorders based on myelin sheath impairment may underlie the neuropathological changes in schizophrenia.But it is unknown whether enhancing remyelination is a beneficial approach to schizophrenia.To investigate this hypothesis,we used clemastine,an FDA-approved drug with high potency in promoting oligodendroglial differentiation and myelination,on a cuprizone-induced mouse model of demyelination.The mice exposed to cuprizone(0.2%in chow) for 6 weeks displayed schizophrenia-like behavioral changes,including decreased exploration of the center in the open field test and increased entries into the arms of the Y-maze,as well as evident demyelination in the cortex and corpus callosum.Clemastine treatment was initiated upon cuprizone withdrawal at 10 mg/kg per day for3 weeks.As expected,myelin repair was greatly enhanced in the demyelinated regions with increased mature oligodendrocytes(APC-positive) and myelin basic protein.More importantly,the clemastine treatment rescued the schizophrenia-like behavioral changes in the open field test and the Y-maze compared to vehicle,suggesting a beneficial effect via promoting myelin repair.Our findings indicate that enhancing remyelination may be a potential therapy for schizophrenia. | Zhifang Li Yangtao He Shuangyi Fan Binbin Sun | 2015 | Neuroscience Bulletin2015，31，5： | 4 |
| 2 | Myelin Deficits Caused by Olig2 Deficiency Lead to Cognitive Dysfunction and Increase Vulnerability to Social Withdrawal in Adult Mice显示文摘Oligodendrocyte (OL) and myelin development are crucial for network integration and are associated with higher brain functions. Accumulating evidence has demonstrated structural and functional impairment of OLs and myelin in serious mental illnesses. However, whether these deficits contribute to the brain dysfunction or pathogenesis of such diseases still lacks direct evidence. In this study, we conditionally deleted Olig2 in oligodendroglial lineage cells (Olig2 cKO) and screened the behavioral changes in adult mice. We found that Olig2 ablation impaired myelin development, which further resulted in severe hypomyelination in the anterior cingulate cortex. Strikingly, Olig2 cKO mice exhibited an anxious phenotype, aberrant responses to stress, and cognitive deficits. Moreover, Olig2 cKO mice showed increased vulnerability to social avoidance under the mild stress of social isolation. Together,these results indicate that developmental deficits in OL and myelin lead to cognitive impairment and increase the risk of phenotypes reminiscent of mental illnesses. | Xianjun Chen Fei Wang Jingli Gan Zhonghua Zhang Xuejun Liang Tao Li Nanxin Huang Xiaofeng Zhao Feng Mei Lan Xiao | 2020 | Neuroscience Bulletin2020，36，4： | 3 |
| 3 | Cuprizone诱导髓鞘损伤再生模型中Sip1的表达变化及其意义显示文摘目的:研究Smad相互作用蛋白1(Sip1)在cuprizone诱导髓鞘损伤再生模型中的表达变化及其意义。方法:通过在饲料中掺入cuprizone喂食C57BL/6小鼠建立髓鞘损伤模型,利用黑金(black gold,BG)染色方法及Western Blot方法,检测髓鞘损伤模型是否建立成功;利用Western Blot方法检测在髓鞘损伤及再生过程中Sip1的表达情况。结果:BG染色方法检测到喂药6周后模型组小鼠与对照组相比,着色显著降低,Western Blot方法检测到模型组小鼠MOG(myelin oligodendrocyte glycoprotein)蛋白表达水平显著降低,GFAP(glial fibrillary acidic protein)蛋白表达水平显著增高,证明髓鞘损伤模型建立成功。在模型建立成功后,停止喂药,改用正常饲料喂养4周后,通过Western Blot检测到模型组小鼠MOG蛋白水平显著恢复,证明该阶段髓鞘已再生。利用Western Blot方法检测髓鞘损伤模型建立阶段及髓鞘再生阶段的Sip1蛋白水平,结果显示与对照组小鼠相比,在髓鞘损伤阶段,模型组小鼠的Sip1蛋白水平显著增加,在髓鞘再生阶段Sip1蛋白水平同样显著增加。结论:Sip1在髓鞘损伤再生过程中具有重要作用,本研究为Sip1作为治疗髓鞘相关疾病的靶点提供了理论依据。 | 余守洋 曹恩瑶 蒋奇阳 陈景海 韦梅 李三华 周亮 邹嘉 | 2016 | 神经解剖学杂志2016，32，1： | 0 |
| 4 | Myelin in development and disease显示文摘Myelin is an evolutionarily novel and important structure for the proper functioning of the vertebrate nervous system.In the central nervous system (CNS), the myelin sheath is elaborated by | Mengsheng Qiu | 2013 | Neuroscience Bulletin2013，29，2： | 0 |
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