DKK1对慢性吗啡和纳洛酮处理的培养海马神经元树突棘的影响  被引量:4

The aflaence or DKK1 on dendritic spines in colrurod hippocampal menrans induced by chronic morphine administration and withdrawal can be relieved by DKK1

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作  者:王建材 冯达云[1] 李洋[1] 王宝[1] 杨倩[1] 高国栋[1] 

机构地区:[1]第四军医大学唐都医院神经外科,西安710038

出  处:《神经解剖学杂志》2016年第1期1-6,共6页Chinese Journal of Neuroanatomy

基  金:国家重点基础研究发展计划(973计划)(2011CB51000);唐都医院科技创新发展基金重大国际合作项目(2013GJHZ001)

摘  要:目的:探讨DKK1作为Wnt通路的抑制剂在吗啡依赖和纳洛酮戒断导致的神经元树突棘发育异常中是否起到一定的保护作用。树突棘是生长在神经元树突上的棘状突起,树突棘的生长与神经元突触可塑性有密切关系。方法:在原代培养的海马神经元上建立慢性吗啡依赖和纳洛酮戒断等模型,运用免疫荧光技术检测神经元树突棘的变化,Western Blot技术和免疫荧光技术检测Wnt通路关键蛋白β-catenin的变化。结果:在慢性吗啡依赖组以及慢性吗啡依赖和纳洛酮戒断组,β-catenin的表达增加并且神经元树突棘发生了明显丢失,而Wnt通路阻断剂DKK1在降低神经元内β-catenin的表达的同时对神经元树突棘的丢失起一定的抑制作用。结论:DKK1通过抑制Wnt通路对吗啡依赖所导致的海马神经元树突棘的丢失有一定作用。Objective: To investigate the relationship between Wnt signaling and the damage of dendritic spine induced by morphine administration. Dendritic spine which may play an important role in synaptie plasticity. Methods: The morphine-dependent and withdrawal models in hippoeampus primary culture ware sernp. Western blot and immunofluoreseenee were wed. Results : The level of β-catenin increased which accompanied by the loss of dendritic spine in morphine group and morphine + naloxone group. However, the DKK1, a Wnt signaling inhibitor which lead to the down-regulation of β-catenin, could protect the dendritic spine from being damaged. Conclusion: Inhibition of Wnt signaling by pkk, may play an important role in the loss of dendritic spine induced by morphine administration.

关 键 词:海马神经元 WNT通路 Β-CATENIN 树突棘 DKK1 

分 类 号:R749.6[医药卫生—神经病学与精神病学]

 

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