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[诱导神经元对β-淀粉样蛋白的形态学抗性]

[Induction of neuron morphological resistance to beta-amyloid].

作者信息

Kokanova N A, Mikhaĭlova G Z, Shtanchaev R Sh, Tiras N R, Moshkov D A

出版信息

Morfologiia. 2012;141(1):23-8.

PMID:22724329
Abstract

The effect of training adaptive vestibular stimulations on goldfish Mauthner neurons (MN) function and three-dimensional morphology was studied in experimental amyloidosis caused by application of aggregated beta-amyloid protein (Abeta25-35). It was found that as compared with control, adapted (trained) MN gained significant resistance to Abeta25-35. Taking into consideration the key role of dopamine in MN adaptation to sensory stimulations, its effect on the development of model amyloidosis was studied. It was shown that the application of dopamine onto MN as well as the increase of its concentration in brain by means of L-dopa protected MN structure and function against pathogenic influence of Abeta25-35. Using electron microscopy it was shown that dopamine protective action on neurons was due to its ability to dissociate polymer amyloid molecules into short inactive fragments.

摘要

研究了训练适应性前庭刺激对由聚集的β-淀粉样蛋白(Abeta25-35)诱导的实验性淀粉样变性中金鱼莫氏神经元(MN)功能和三维形态的影响。结果发现,与对照组相比,适应(训练)后的MN对Abeta25-35具有显著的抗性。考虑到多巴胺在MN对感觉刺激适应中的关键作用,研究了其对模型淀粉样变性发展的影响。结果表明,将多巴胺应用于MN以及通过左旋多巴增加其在脑中的浓度可保护MN的结构和功能免受Abeta25-35的致病影响。利用电子显微镜显示,多巴胺对神经元的保护作用是由于其能够将聚合物淀粉样分子解离成短的无活性片段。

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