Brain research
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In this study, our objective is to investigate the effects of mannitol and 7.5% hypertonic saline (HS) therapy on the levels of malondialdehyde (MDA), catalase and glutathione peroxidase (GSH-Px) in the early stages of experimental head traumas in rats. Rats included in the study were divided into four groups: Group I Control, Group II Trauma, Group III Mannitol, and Group IV 7.5% Hypertonic Saline. Rats in Group II were subject to head trauma only. ⋯ By contrast, in the mannitol group, MDA, catalase and GSH-Px levels were lower than the levels in the trauma group, and these reductions were statistically significant (p<0.05). The MDA, catalase and GSH-Px levels of the 7.5% HS group were lower than those of the trauma group; however, this reduction was not statistically significant. It was concluded that mannitol and 7.5% HS therapies that are used to reduce intracranial pressure and to increase the use of catalase, an antioxidant enzyme, and GSH-Px, are likely to reduce cellular damage by reducing the formation of MDA, the levels of which are known to be indicative of cellular level oxidant damage.
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Two different mechanisms by which capsaicin blocks voltage-gated sodium channels (VGSCs) were found by using knockout mice for the transient receptor potential V1 (TRPV1(-/-)). Similar with cultured rat trigeminal ganglion (TG) neurons, the amplitude of tetrodotoxin-resistant (TTX-R) sodium current was reduced 85% by 1 muM capsaicin in capsaicin sensitive neurons, while only 6% was blocked in capsaicin insensitive neurons of TRPV1(+/+) mice. The selective effect of low concentration capsaicin on VGSCs was reversed in TRPV1(-/-) mice, which suggested that this effect was dependent on TRPV1 receptor. ⋯ That is, firstly, both blockages are concentration-dependent and revisable. Secondly, being accompanied with the reduction of amplitude, voltage-dependent inactivation curve shifts to hyperpolarizing direction without a shift of activation curve. Thirdly, use-dependent blocks are induced at high stimulus frequency.
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This study was performed to determine whether dexamethasone (DEX) had an effect on ATP-sensitive potassium channels (K(ATP) channels) in blood-brain tumor barrier (BTB). Using a rat brain glioma model, we found that DEX could significantly increase the expression of K(ATP) channels protein at tumor sites. ⋯ DEX significantly decreased the BTB permeability, but it did not reduce bradykinin-mediated BTB permeability increase, which were significantly attenuated by the K(ATP) channel antagonist glibenclamide. This led to the conclusion that DEX-mediated change in BTB permeability is, at least partly, due to accelerated formation of K(ATP) channel, an important target in the biochemical regulation of this process.
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Previous positron emission tomography (PET) studies have shown greater medial temporal lobe activation (MTL) for associative memory encoding relative to deep item-oriented encoding. Greater MTL activation has also been reported for associative novelty detection. Although it has been suggested that these patterns of MTL activation could reflect the creation of novel associations into memory, it is unclear whether associative encoding and associative novelty detection rely on the same MTL substructures. ⋯ The orthogonal contrast between arbitrary and related pairs revealed greater activation in the left parahippocampal region, but no significant interaction between the type of encoding (associative or item oriented) and the type of pairs (arbitrary or semantically related) was observed in the medial temporal lobe (MTL). These results suggest that both associative processing and associative novelty detection can activate the MTL. Most importantly, this study suggests that associative processing can activate the MTL regardless of the pre-existence of an association between the items of a pair.