The main symptoms of Alzheimer's disease (AD) is the loss of learning and memory ability, of which biological basis is synaptic plasticity. Aluminium has been found to cause changes in synaptic plasticity, but its molecular mechanism was unclear. In this study, Sprague-Dawley rats were injected with aluminium maltol (Al(mal)₃) through the lateral ventricle to establish an AD-like model. Y-maze, electrophysiological measurements, Golgi staining, scanning electron microscopy, quantitative real-time polymerase chain reaction, and western blot techniques were used to investigate regulation of the metabolic glutamate receptor 1 (mGluR1) in synaptic plasticity impairment induced by Al(mal)₃. The results showed that Al(mal)₃ inhibited the induction and maintenance of long-term potentiation in the hippocampal CA1 region. During this process, the expression of mGluR1 was up-regulated and it inhibited the expression and phosphorylation of the N-methyl-D-aspartic acid receptors (NMDARs). This mainly affected NMDAR1 and NMDAR2B but did not affect protein kinase C expression.

阿尔茨海默氏病（AD）的主要症状是学习和记忆能力的丧失，其生物学基础是突触可塑性。已经发现铝引起突触可塑性的改变，但是其分子机理尚不清楚。在这项研究中，Sprague-Dawley大鼠通过侧脑室注射了麦芽酚铝（Al（mal）₃），以建立AD样模型。使用Y迷宫，电生理测量，高尔基染色，扫描电子显微镜，定量实时聚合酶链反应和Western印迹技术来研究代谢谷氨酸受体1（mGluR1）在Al（mal）诱导的突触可塑性损伤中的调节作用。₃。结果表明，Al（mal）₃抑制海马CA1区长时程增强的诱导和维持。在此过程中，mGluR1的表达上调，并抑制了N-甲基-D-天冬氨酸受体（NMDARs）的表达和磷酸化。这主要影响NMDAR1和NMDAR2B，但不影响蛋白激酶C的表达。