Altered hippocampus synaptic function in selenoprotein P deficient mice

• Main Authors: Peters Melinda M, Hill Kristina E, Burk Raymond F, Weeber Edwin J
• Format: Article
• Language: English
• Published: BMC 2006-09-01
• Series: Molecular Neurodegeneration
• Online Access: http://www.molecularneurodegeneration.com/content/1/1/12

<p>Abstract</p> <p>Selenium is an essential micronutrient that function through selenoproteins. Selenium deficiency results in lower concentrations of selenium and selenoproteins. The brain maintains it's selenium better than other tissues under low-selenium conditions. Recently, the selenium-containing protein selenoprotein P (Sepp) has been identified as a possible transporter of selenium. The targeted disruption of the selenoprotein P gene (<it>Sepp1</it>) results in decreased brain selenium concentration and neurological dysfunction, unless selenium intake is excessive However, the effect of selenoprotein P deficiency on the processes of memory formation and synaptic plasticity is unknown. In the present studies <it>Sepp1</it>(-/-) mice and wild type littermate controls (<it>Sepp1</it>(+/+)) fed a high-selenium diet (1 mg Se/kg) were used to characterize activity, motor coordination, and anxiety as well as hippocampus-dependent learning and memory. Normal associative learning, but disrupted spatial learning was observed in <it>Sepp1</it>(-/-) mice. In addition, severe alterations were observed in synaptic transmission, short-term plasticity and long-term potentiation in hippocampus area CA1 synapses of <it>Sepp1</it>(-/-) mice on a 1 mg Se/kg diet and <it>Sepp1</it>(+/+) mice fed a selenium-deficient (0 mg Se/kg) diet. Taken together, these data suggest that selenoprotein P is required for normal synaptic function, either through presence of the protein or delivery of required selenium to the CNS.</p>