Based on the radioactivity in aqueous, total lipid, neutral lipid and phospholipid

fractions, volume of distribution (V(D), mu l/g) was calculated. The V(D) between CRT0066101 clinical trial (14)C-EPA- and (14)C-DHA-perfused samples was not statistically different for total lipid, neutral lipids or total phospholipids. However, the V(D) of (14)C-EPA in the aqueous fraction was 2.5 times higher than that of (14)C-DHA (p = 0.025), suggesting a more extensive beta-oxidation than DHA. Furthermore, radiolabeled palmitoleic acid, a fatty acid that can be synthesized de novo, was detected in brain phospholipids from (14)C-EPA but not from (14)C-DHA-perfused mice suggesting that beta-oxidation products of EPA were recycled into endogenous fatty acid biosynthetic pathways. These findings suggest that low levels of EPA in brain phospholipids compared to DHA may be the result of its rapid beta-oxidation upon uptake by the brain. (C) 2009 Elsevier Ltd. All rights reserved.”
“Lithium, a simple cation, is the mainstay treatment of bipolar disorder. Deficient synaptic plasticity is considered one important mechanism of this disease. Lithium inhibits glycogen synthase

kinase-3beta (GSK-3 beta), which is involved in the regulation of synaptic plasticity. In animal preparations, inhibition of GSK-3 beta by lithium up-regulated long-term potentiation (LTP) of excitatory synapses but downregulated selleck chemicals long-term depression (LTD). The effects of lithium on plasticity in the human brain are unexplored. We tested the effects of a single oral dose of 900 mg of lithium on LTP-/LTD-like plasticity in human motor cortex induced by established paired associative transcranial magnetic stimulation Dichloromethane dehalogenase (PAS(LTR) PAS(LTD)) protocols. We studied 10 healthy adults in a placebo-controlled double-blind randomized crossover design. PAS-induced plasticity was indexed by change in motor evoked potential amplitude recorded in a hand muscle. In the placebo session, subjects were stratified, according to the known

variability of the PAS(LTP) response, into PAS(LTP) ‘LTP’ responders’ and PAS(LTP) ‘LTD responders’ (n = 5 each). Lithium did not affect the PAS(LTP)-induced LTP-like plasticity in the ‘LIP responders’, but switched the PAS(LTP)-induced LTD-like plasticity in the ‘LTD responders’ to LTP-like plasticity. In contrast, lithium had no effect on the PAS(LTD)-induced LTD-like plasticity in the ‘LTD responders’. We provide first-time evidence that lithium significantly modulates brain stimulation induced plasticity in human cortex. The switch from LTD- to LTP-like plasticity is best explained by the inhibitory action of lithium on GSK-3 beta. This conclusion is necessarily circumstantial because GSK-3 beta activity was not directly measured. We discuss that other important plasticity-related modes actions of lithium cannot explain our findings. (C) 2012 Elsevier Ltd. All rights reserved.