N-Methyl-D-Aspartate Receptors Mediate Synaptic Plasticity Impairment of Hippocampal Neurons Due to Arsenic Exposure

Abstract

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.

Keywords: Arsenic; NMDA receptors; Neurotoxicity; Synaptic plasticity.