Background Lead(Pb),as a widespread environmental pollutant,is known to cause a wide range of neurotoxic effects,including decreased intelligence quotient,cognitive deficits,poor attention span,and increased *** has l...
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Background Lead(Pb),as a widespread environmental pollutant,is known to cause a wide range of neurotoxic effects,including decreased intelligence quotient,cognitive deficits,poor attention span,and increased *** has long been recognized as a neurodevelopmental *** blood-brain barrier(BBB) and blood-cerebrospinal fluid barrier(BCB) are known to be targets of Pb neurotoxicity. Brain capillary endothelial cells with tight junctions(TJs) between adjacent cells, astrocyte end feet, and pericytes within the capillary basement constitute the structural basis of the BBB. Choroid plexus epithelial cells with tight junctions(TJs) between adjacent cells constitute the structural basis of the ***, the underlying mechanisms of Pb-induced reduction of TJ proteins of BBB and BCB are still *** way Pb enters into the brain parenchyma or cerebrospinal fluid can be classified into two categories: intercellular regions after breakdown TJ proteins and Pb transporter in the endothelial/epithelial cell bodies. Recently, hemichannels of Connexin 43(Cx43), the most ubiquitously expressed gap junction proteins in the BBB and BCB, were found to be important pathways for many substances. In previous study, Cx43 expression was enhanced in the hippocampus, a major target of Pb-induced neurotoxicity, implying that Pb may accumulate in the hippocampus via Cx43 *** is nonreceptor protein tyrosine kinases that mediates the integrin signaling on the focal adhesion complex at the cell-toextracellular matrix interface. Src kinase activity is required for both assembly and disassembly of TJ proteins in different epithelial cells. In addition, Src has long been known to interact with and phosphorylate Cx43 to promote downregulation of GJ communication and cause GJ disassembly,even channel closure. Src phosphorylation was found to increase greater than other kinases in brain microvessels after Pb exposure by using a phosphoprotein antibody *** This
[目的]本部分研究利用AD模型大鼠,观察AD模型大鼠是否出现睡眠片段化。其次,为了加速睡眠片段化对AD病理改变的病理进程,本研究使用了睡眠干扰(sleep interruption,SI)对AD模型大鼠进行睡眠片段化处理,观察海马脑组织间液β淀粉样蛋白(ISF A β)浓度变化。[方法]选用雄性成年Sprague-Dawley大鼠,麻醉后同时安放脑电记录电极和微透析引导管及基座。首先将大鼠分为模型组和假手术组,模型组经1周恢复期后在双侧海马注射A β 25-35制作AD模型,假手术组同样位置注射生理盐水。两组于造模后进行Morris水迷宫行为学检测。两组收集脑电数据。大鼠AD造模验证后,收集海马脑ISF A β数据作为基线。再进行分组,一组进行睡眠干扰(SI),目的是加速进行睡眠片段化,该组为SI组,共7天。另一组为运动对照组(EC),保证两组大鼠运动量相同。恢复3天后,收集海马脑组织间液,检测海马ISF A β。睡眠脑电指标采用SleepSign软件自动分析后人工修正,脑ISF中的Aβ浓度由ELISA法测定。
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