Deficiency but Not Supplementation of Selenium Impairs the Hippocampal Long-Term Potentiation and Hippocampus-Dependent Learning.

Among the chemical factors that have been implicated in the etiology of dementia, recent concern has focused on both increased and decreased exposure to the metalloid selenium (Se). This report describes the molecular, behavioral, and electrophysiological analysis of rats that were fed with Se-free chow and Se-enriched tap water for 21 days. Three groups were produced, feeding them on a deficient diet with different Selenium content. Hippocampus-dependent spatial learning was measured using the water maze. Long-term potentiation (LTP) was recorded in the hippocampal dentate gyrus to assess how memory is formed at the cellular level. Hippocampal Se levels were measured in trained rats by using inductively coupled plasma mass spectrometry. Phosphorylated and total tau levels were measured in whole hippocampus by Western blot. An impairment of learning of rats feeding with Se-deficient diet was accompanied by attenuated LTP, and increased ratio of p231Tau-to- and decreased ratio of p416Tau-to-Tau in the non-stimulated hippocampus, despite no significant change was observed in Se levels of hippocampus and plasma. Se supplementation resulted in an increase in both tissues and an increase in the ratio of p231Tau-to-Tau in the non-stimulated hippocampus but did not change learning performance and LTP. Despite impaired learning and LTP, no group differed in probe trial and in the fraction of phosphorylated tau in LTP-induced hippocampus. Reduced level of selenium would probably result in reduced synaptic plasticity as well as impairment of learning ability, suggesting requirement of Se for normal synaptic function.