砷暴露导致海马神经元突触可塑性损伤的机制：N-甲基-D-天冬氨酸受体介导作用。
N-Methyl-D-Aspartate Receptors Mediate Synaptic Plasticity Impairment of Hippocampal Neurons Due to Arsenic Exposure.
机构信息
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, National Health Commission & Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University (23618504), Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health, Harbin 150081, China.
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, National Health Commission & Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University (23618504), Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health, Harbin 150081, China.
出版信息
Neuroscience. 2022 Aug 21;498:300-310. doi: 10.1016/j.neuroscience.2022.07.017. Epub 2022 Jul 26.
Endemic arsenism is a worldwide health problem. Chronic arsenic exposure results in cognitive dysfunction due to arsenic and its metabolites accumulating in hippocampus. As the cellular basis of cognition, synaptic plasticity is pivotal in arsenic-induced cognitive dysfunction. N-methyl-D-aspartate receptors (NMDARs) serve physiological functions in synaptic transmission. However, excessive NMDARs activity contributes to exitotoxicity and synaptic plasticity impairment. Here, we provide an overview of the mechanisms that NMDARs and their downstream signaling pathways mediate synaptic plasticity impairment due to arsenic exposure in hippocampal neurons, ways of arsenic exerting on NMDARs, as well as the potential therapeutic targets except for water improvement.
地方性砷中毒是一个全球性的健康问题。由于砷及其代谢物在海马体中积累，慢性砷暴露会导致认知功能障碍。作为认知的细胞基础，突触可塑性在砷诱导的认知功能障碍中起着关键作用。N-甲基-D-天冬氨酸受体（NMDARs）在突触传递中发挥生理功能。然而，过量的 NMDAR 活性会导致神经毒性和突触可塑性障碍。在这里，我们综述了 NMDAR 及其下游信号通路介导砷暴露致海马神经元突触可塑性障碍的机制、砷作用于 NMDAR 的方式，以及除改善水质之外的潜在治疗靶点。
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