Umareddy, A. Chao, A. Sampath, F. Gu, and S. G. Vasudevan, J. Gen. Virol. 87:2605-2614,2006). Collectively, the results suggest that the identified inhibitor targets the DENV NS4B protein, leading to a defect in viral RNA synthesis.”
“Both in vivo and in vitro studies have shown that neurosteroids promote learning and memory by modulating synaptic functions in the hippocampus. However, we do not know to what degree endogenously synthesized neurosteroids contribute to the hippocampal synaptic functions. Cytochrome P450scc is the enzyme that converts cholesterol to pregnenolone (PREG), which is required for the biosynthesis of all other neurosteroids. To
investigate the physiological roles of endogenous neurosteroids in synaptic functions, we electrophysiologically examined the effects of aminoglutethimide Mocetinostat in vitro (AG), a selective
VEGFR inhibitor inhibitor of P450scc, on the synaptic transmission and plasticity in the dentate gyrus of rat hippocampal slices. The application of AG (100 mu M) decreased the slope of the field excitatory postsynaptic potentials (fEPSPs) in granule cells by 20-30% in 20 min through the modulation of postsynaptic AMPA receptors, while it did not affect the presynaptic properties, including the paired-pulse ratio and the probability of glutamate release from presynaptic terminals. The AG-induced depression was nearly completely rescued by exogenously applied 500 nM PREG or by 1 nM dehydroepiandrosterone sulfate (DHEAS), one of the neurosteroids synthesized from PREG, suggesting that the AG-induced depression was caused by the loss of DHEAS. AG also reduced NMDA receptor activity, and suppressed high-frequency stimulation (HFS)-induced long-term potentiation (LTP). These findings provide novel evidence Selleck Idelalisib that the endogenous neurosteroids locally synthesized in the brain are required to maintain the normal excitatory synaptic transmission and plasticity in the dentate gyrus of the rat hippocampus. (C) 2012 Elsevier Ltd. All rights reserved.”
“Objective: To investigate alternative hypothetical
models that could clarify the relationship between depressive symptoms and serum cholesterol fractions, i.e., high-density lipoprotein (HDL) and low-density lipoprotein (LDL). It was hypothesized that the impact of the depressive symptoms on cholesterol fractions is mediated through health behavior and body mass index, and at the same time there would be a direct link from depression to cholesterol. Methods: The study sample consisted of 893 middle-age men who participated in a trial aimed at preventing the metabolic syndrome, Type 2 diabetes and cardiovascular diseases. Serum cholesterol was measured by the enzymatic method. Participants completed self-report questionnaires assessing health behavior and depressive symptoms. Results: Depressive symptoms consistently correlated statistically significantly with adverse lifestyle factors and, as hypothesized, positively with HDL.