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β淀粉样蛋白1-42对大鼠海马神经元树突棘的影响
引用本文:耿丹丹,张润娇,高燕京,师晓帆,张钰佳,王磊.β淀粉样蛋白1-42对大鼠海马神经元树突棘的影响[J].神经解剖学杂志,2021(1):55-60.
作者姓名:耿丹丹  张润娇  高燕京  师晓帆  张钰佳  王磊
作者单位:;1.河北医科大学人体解剖学教研室
基金项目:河北省高层次人才资助项目(B2016003023);河北省基础研究专项(H2020206299,C2020206037)。
摘    要:目的:研究β淀粉样蛋白1-42(Aβ1-42)对于原代培养的大鼠海马神经元树突棘形态和数量的影响。方法:将原代培养的新生大鼠海马神经元随机分为对照组(control)和Aβ1-42处理组(Aβ1-42),用浓度为500nmol/L的Aβ1-42处理细胞,应用免疫荧光染色检测树突棘上大脑发育调节蛋白(drebrin)的表达,分析Aβ1-42处理不同时间对海马神经元树突棘形态和密度改变的影响。结果:随着Aβ1-42处理时间的增加,drebrin免疫荧光强度明显降低,树突棘形态和密度发生显著变化。对照组树突棘头靠近树突干,多为短粗型或蘑菇型,具有成熟树突棘的典型特征。Aβ1-42处理组丝状伪足样细长树突棘显著增加,异常增长的树突棘数量增多,树突棘密度显著降低。结论:Aβ1-42可明显降低原代培养海马神经元内的drebrin免疫荧光强度和树突棘数量,为进一步探讨Aβ1-42诱导树突棘退行性变的机制提供了直接的细胞生物学依据。

关 键 词:β淀粉样蛋白1-42  树突棘  大脑发育调节蛋白  阿尔茨海默病  大鼠

Effects of amyloid-beta 1-42 on dendritic spines of hippocampal neurons in rats
Geng Dandan,Zhang Runjiao,Gao Yanjing,Shi Xiaofan,Zhang Yujia,Wang Lei.Effects of amyloid-beta 1-42 on dendritic spines of hippocampal neurons in rats[J].Chinese Journal of Neuroanatomy,2021(1):55-60.
Authors:Geng Dandan  Zhang Runjiao  Gao Yanjing  Shi Xiaofan  Zhang Yujia  Wang Lei
Institution:(Department of Human Anatomy,Hebei Medical University,Shijiazhuang 050017,China)
Abstract:Objective:To investigate the effect of amyloid-beta 1-42(Aβ1-42)on the morphology and number of dendritic spines in primary cultured hippocampal neurons.Methods:The hippocampal tissues of neonatal SD rats within24 hours were cultured for primary neurons.Neurons were randomly divided into control group and Aβ1-42 group.And then were treated with 500 nmol/L of Aβ1-42.The dendritic spines were labeled with immunofluorescence staining of development regulation brain protein(drebrin),and the morphological and density changes of dendritic spines were analyzed.Results:With the increase of Aβ1-42 treatment time,the immunofluorescence intensity of drebrin decreased significantly,as well as dramatic changes in spine morphology and density.The control group showed short protrusions with spine heads close to the shaft,mostly stubby and mushroom types,with typical characteristics of mature spines.In Aβ1-42 treatment groups,thin filopodia-like dendritic spines increased obviously,the number of abnormal longer spines increased,and the density of spines decreased significantly.Conclusion:Aβ1-42 significantly reduced the intensity of drebrin immunofluorescence and the number of dendritic spines in mature hippocampal neurons.This study provides a direct cell biological basis for exploring the mechanism of spine degeneration induced by Aβ1-42.
Keywords:amyloid-beta 1-42  dendritic spine  drebrin  Alzheimer’s disease  rat
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