Manganese (Mn) is an environmental pollutant having a toxic effect on Parkinson's disease, with significant damage seen in the neurons of basal ganglia. Hence, Mn pollution is a public health concern. A Sprague-Dawley rat model was used to determine the damage to basal nuclei, and the effect of Mn intake was detected using the Morris water maze test and transmission electron microscopy. The SH-SY5Y cell line was exposed to Mn, and downstream signaling was assessed to determine the mechanism of toxicity. Mn exposure injured neurons, repressing GABAAR receptors and inducing GABABR receptors. The synergistic effect of the GABABR receptor and Kir6.1-SUR1 or Kir6.2-SUR1 was found to be one of the potential factors for the secretion of α-synuclein. The accumulation of α-synuclein regulated downstream factors calmodulin (CAM)\cAMP response element-binding protein (CREB), thereby impairing learning and memory. Other genes downstream of CREB, rather than the feedback regulation of CREB, and brain-derived neurotrophic factor might also be involved.

中文翻译：

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锰通过 ATP 敏感 K(+) 通道和 GABA 受体积累 α-突触核蛋白引起的神经损伤


锰（Mn）是一种环境污染物，对帕金森病具有毒性作用，对基底神经节神经元有显着损害。因此，锰污染是一个公共卫生问题。使用Sprague-Dawley大鼠模型来确定对基底核的损伤，并使用Morris水迷宫试验和透射电子显微镜检测锰摄入的影响。将 SH-SY5Y 细胞系暴露于 Mn，并评估下游信号传导以确定毒性机制。锰暴露会损伤神经元，抑制 GABAAR 受体并诱导 GABABR 受体。 GABABR受体与Kir6.1-SUR1或Kir6.2-SUR1的协同作用被发现是α-突触核蛋白分泌的潜在因素之一。 α-突触核蛋白的积累调节下游因子钙调蛋白（CAM）\cAMP反应元件结合蛋白（CREB），从而损害学习和记忆。 CREB下游的其他基因，而不是CREB的反馈调节，以及脑源性神经营养因子也可能参与其中。