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作 者:Xin Huang Jia Sun Tong Zhao Kuiwu Wu Kazutada Watanabe Zhi-Cheng Xiao Ling-ling Zhu Ming Fan
出 处:《生理通讯》2014年第3期70-77,共8页
摘 要:2013年10月12—13日中国生理学会张锡钧基金会第十二届全国青年优秀生理学学术论文交流会在湖南长沙顺利召开。由各省生理学会推荐的37名参赛选手的论文参加评选,会议展示了选手们近3年来在生理学研究方面所取得的最新研究成果。经过专家对参评者论文和现场报告的综合评判,评出一等奖、二等奖、三等奖、特别奖、最佳表达奖、最佳答辩奖和最佳图表奖共11名。从2013年第6期开始,《生理通讯》将陆续转载获奖者的参评论文各一篇,以飨读者。Background and Purpose: NB-3 is a member of the F3/contactin family of neural recognition molecules, which are crucial for cell morphogenesis and motility. NB-3 is expressed in neurons and plays an important role in axonal extension and neuronal survival. However, the role of NB-3 in cerebral ischemic injury remains unknown. Methods: Adult male wild-type and NB-3 knockout (KO) mice were subjected to ischemic injury by unilateral middle cerebral carotid artery occlusion for 3h, 6h and 12h. Ischernic infarction volumes were then determined by 2, 3, 5-triphenyltetrazolium chloride staining. Neurological dysfunction analysis was also performed. Primary culture of neuronal cells from wild-type and knockout animals were also used for analysis of neuronal survival and neurite outgrowth. Results: NB-3 expression in the ischemic hemisphere was decreased after transient middle cerebral artery occlusion (MCAO). NB-3-KO mice developed a 2.6-fold larger infarct volume and exhibited increased neurological deficit scores after transient MCAO compared with control mice. Substrate with NB-3 promoted neuronal survival and neurite outgrowth in vitro, while neurite outgrowth and neuronal survival were significantly reduced in NB-3-deficient neurons. In addition, NB-3 deficiency renders neurons more susceptible to oxygen-glucose deprivation (OGD)-induced damage and NB-3 as substrate could partially via homophilic mechanisms. Conclusions: These data demonstrate that NB-3 deficiency may aggravate brain damage after MCAO by impairing neuronal survival and neurite growth.
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