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首页> 外文期刊>Biochemistry >In vivo Injected Mitochondria-Targeted PlastoquinoneAntioxidant SkQR1 Prevents β-Amyloid-Induced Decayof Long-Term Potentiation in Rat Hippocampal Slices
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In vivo Injected Mitochondria-Targeted PlastoquinoneAntioxidant SkQR1 Prevents β-Amyloid-Induced Decayof Long-Term Potentiation in Rat Hippocampal Slices

机译:体内注射线粒体靶向的醌醌抗氧化剂SkQR1防止β-淀粉样蛋白诱导的大鼠海马切片长期增生衰减。

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摘要

Addition of 200 nM β-amyloid 1-42 (Abeta) to a rat hippocampal slice impairs the induction of a long-term post-tetanic potentiation (LTP) of population spike (PS) in pyramidal neurons of the CA1 field of hippocampus. Intraperitoneal injection into the rat of the mitochondria-targeted plastoquinone derivative SkQRl (1 umol/kg of weight given 24 h before the slices were made) abolishes the deleterious effect of Abeta on LTP. These data demonstrate that SkQRl therapy is able to compensate the Abeta-induced impairments of long-term synaptic plasticity in the hippocampus, which are the main cause of loss of memory and other cognitive functions associated with Alzheimer's disease.
机译:向大鼠海马切片中添加200 nMβ-淀粉样蛋白1-42(Abeta)会削弱海马CA1区域锥体神经元中种群峰值(PS)的长期强直后增强(LTP)诱导能力。向大鼠腹膜内注射线粒体定位的质体醌衍生物SkQR1(在切片前24小时给予1 umol / kg体重)消除了Abeta对LTP的有害作用。这些数据表明,SkQR1疗法能够补偿Abeta引起的海马的长期突触可塑性损伤,这是记忆丧失和与阿尔茨海默氏病有关的其他认知功能的主要原因。

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