期刊
NEUROSCIENCE
卷 498, 期 -, 页码 300-310出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2022.07.017
关键词
Arsenic; NMDA receptors; Synaptic plasticity; Neurotoxicity
Chronic arsenic exposure can lead to endemic arsenism and cognitive dysfunction, with NMDARs and their downstream signaling pathways playing a crucial role in synaptic plasticity impairment caused by arsenic exposure. Apart from improving water quality, potential therapeutic targets need to be identified.
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 exi-totoxicity 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 hip-pocampal neurons, ways of arsenic exerting on NMDARs, as well as the potential therapeutic targets except for water improvement. (c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
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