Selenium deficiency increases susceptibility to glutamate‐induced excitotoxicity

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Abstract
SPECIFIC AIMSExcitotoxic brain lesions, such as stroke and epilepsy, lead to increasing destruction of neurons hours after the insult. The deadly cascade of events involves detrimental actions by free radicals and the activation of proapoptotic transcription factors, which finally results in neuronal destruction. We provide direct evidence that the essential trace element selenium has a pivotal role in neuronal susceptibility to excitotoxic lesions and seizure activity.PRINCIPAL FINDINGS1. Selenium prevents glutamate-induced cell deathWe first treated the hippocampal neuronal cell line HT22 with selenium in form of selenite (Na2SeO3). Selenite concentrations of up to the micromolar range were tolerated by neurons without any influence on cell viability, whereas higher amounts of selenium led to cell death (Fig. 1⤻ a). Excitotoxic conditions were induced in neurons by treatment with an excess of glutamate, the most abundant excitatory neurotransmitter in the brain. Glutamate treatment reduced cell survival...