Department of Brain Research, Research Center of Neurology, Russian Academy of Medical Sciences, Pereulok Obukha 5, 105064 Moscow, Russia.
Biochemistry (Mosc). 2011 Dec;76(12):1367-70. doi: 10.1134/S0006297911120108.
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 SkQR1 (1 µmol/kg of weight given 24 h before the slices were made) abolishes the deleterious effect of Abeta on LTP. These data demonstrate that SkQR1 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.
向大鼠海马切片中添加 200 nMβ-淀粉样蛋白 1-42（Abeta）会损害 CA1 场锥体神经元群体峰电位（PS）的长时程突触后增强（LTP）的诱导。将线粒体靶向质体醌衍生物 SkQR1（在切片制备前 24 小时给予 1µmol/kg 的体重腹腔内注射）注入大鼠体内可消除 Abeta 对 LTP 的有害影响。这些数据表明，SkQR1 治疗能够补偿 Abeta 诱导的海马体长期突触可塑性的损伤，这是与阿尔茨海默病相关的记忆丧失和其他认知功能丧失的主要原因。
