题目：New findings from cuprizone model supporting a putative role of dysfunctional oligodendrocytes in the pathogenesis of schizophrenia
报告人：许海云教授
报告人简介：
许海云博士，汕头大学医学院特聘教授。1996年获中国协和医科大学博士学位，主修神经生物学。1996-2002年先后在美国威斯康辛医学院和加拿大萨斯克彻温大学做博士后研究。2003-2006年在萨斯克彻温大学医学院神经精神病学研究中心任讲师（Research Associate）。2006-2011年在美国南伊利偌依大学医学院解剖学系任助理教授（Assistant Professor）。主要从事神经精神药理学和生物精神病学研究。首先以实验证据证实了少突胶质细胞和脑白质损伤在动物（C57BL/6 mouse）引起精神分裂症样行为改变，而且这些改变能被抗精神分裂药（Antipsychotics）预防或减轻。发表的系列研究论文为精神分裂症的病理生理和治疗开辟了一个新领域。最近受Schizophrenia Research and Treatment杂志社邀请主编了一期特刊Oligodendrocytes in Schizophrenia。迄今共发表了40多篇科研论文，影响因子超过100，被引用1000多次。为Brain Research, Journal of Neurochemistry, Neuropsychopharmacology, Neurosignal 等杂志审稿。2011年九月回国受聘汕头大学医学院特聘教授。
时间：2015年10月21日 星期三 9:00-12:00
地点： Room 1113, Wangkezhen Building
邀请人：李量
摘要：
Cuprizone is a copper chelator able to selectively induce demyelination and oligodendrocyte loss, followed by spontaneous remyelination, in brains of rodents. Thus the cuprizone mouse has been widely used as an animal model for demyelination and remyelination research. Recent studies, however, have examined the behavioral changes in the cuprizone-exposed mice, including those relevant to psychiatric diseases. The serial research in my lab has established the cuprizone mouse as a novel animal model of schizophrenia for which human studies have provided observational data suggesting a putative role of dysfunctional oligodendrocytes in the pathogenesis of this mental disorder, including white matter abnormalities, alterations in the structure and functions of myelin-related genes, and schizophrenia behaviors seen in patients with white matter diseases. Our experimental data not only showed behavioral changes of the emotional and cognitive functions in the cuprizone-exposed mice, but also demonstrated the protective effects of certain existing antipsychotics on the cuprizone-induced behavioral changes and white matter alterations in the brain which mimic those seen in patients with schizophrenia. More recent studies in my lab provided evidence of neuonal dysfunctions preceding the obvious demyelination and proposed a mechanism of the dysrupption of neuron-glia integration for schizophrenia.