Brain research
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The current study used event-related potentials (ERPs) and masked repetition priming to examine the time-course of picture processing. We manipulated the stimulus-onset asynchrony (110 ms, 230 ms, 350 ms, and 470 ms) between repeated and unrepeated prime-target pairs while holding the prime duration constant (50 ms) (Experiment 1) as well as the prime durations (30 ms, 50 ms, 70 ms, and 90 ms) (Experiment 2) with a constant SOA of 110 ms in a masked repetition priming paradigm with pictures. The aim of this study was to further elucidate the mechanisms underlying previously observed ERP components in masked priming with pictures. We found that both the N/P190 and N400 are modulated by changes in prime duration and SOA, however, it appears that longer prime exposure rather than a longer SOA leads to more in-depth processing as indexed by larger N400 effects.
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Infection and inflammation leading to injury or death of pre-oligodendrocytes (preOLs) is one of the principal initiating mechanisms in the pathogenesis of preterm periventricular leukomalacia (PVL). The present study explores the possible protective effect of curcumin against the toxicity of lipopolysaccharide (LPS)-activated microglia on preOLs in vitro and in vivo. In vitro, preOLs in coculture with microglia exhibited increased apoptosis after exposure to LPS. ⋯ Treatment with curcumin either 1h before or immediately after LPS injection significantly ameliorated white matter injury and loss of preOLs, decreased activated microglia, and inhibited microglial expression of iNOS and translocation of p67phox and gp91phox to the microglial cell membranes in neonatal rat brains following LPS injection. These results suggest that curcumin has a protective effect on infection-driven white matter injury, which is associated with suppression of iNOS and NOX activation. Consequently, curcumin may have potential as a protective agent against immature white matter injury.
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Blockade of serotonergic receptors in the lateral parabrachial nucleus (LPBN), via bilateral injections of nonselective 5-hydroxytryptamine (5-HT)(1/2)-receptor antagonist, methysergide causes a robust sodium appetite. Our aim was to elucidate which brain regions are activated when serotonergic pathways to the LPBN are blocked and combined with subcutaneous injection of isoproterenol causing a salt appetite. In the experimental group, conscious rats were administered methysergide (4 microg/0.2 microl) injected bilaterally into the LPBN. ⋯ Bilateral injections of methysergide into the LPBN followed by subcutaneous isoproterenol induced a strong intake of 0.3M NaCl (p<0.01) compared with all controls. Greater numbers of c-Fos-positive stained nuclei were observed in all brain regions assessed. The extended amygdala is rich in AT(1) receptors and ablation of these regions has been shown to reduce sodium appetite; therefore, neurons in these sites, and to a lesser extent the lamina terminalis, are likely primary targets of an inhibitory mechanism arising from the LPBN that acts to modulate sodium appetite.
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Mammalian circadian rhythms are generated by a network of transcriptional and translational loops in the expression of a panel of clock genes in various brain and peripheral sites. Many of the output rhythms controlled by this system are significantly affected by ageing, although the mechanisms of age-related circadian dysfunction remain opaque. The aim of this study was to investigate the effect of aging on the daily oscillation of two clock gene proteins (CLOCK, BMAL1) in the mouse brain. ⋯ We report novel rhythmic expression of CLOCK and BMAL1 in a number of extra-SCN sites in the young mouse brain, including the hippocampus, amygdala and the paraventricular, arcuate and dorsomedial nuclei of the hypothalamus. Aging altered the amplitude and/or phase of expression in these regions. These results indicate hitherto unreported expression patterns of CLOCK and BMAL1 in non-SCN brain circadian oscillators, and suggest that alterations of these patterns may contribute to age-related circadian dysfunction.
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Mammalian target of rapamycin (mTOR) controls protein translation and has an important role in the mechanism of pain hypersensitivity under persistent pain conditions. However, its expression and localization in pain-related regions of the nervous system is not completely understood. Here, we examined the expression and distribution of mTOR, eukaryotic initiation factor 4E-binding protein1/2 (4E-BP1/2), p70 ribosomal S6 protein kinase (p70S6K), and their phosphorylated (active) counterparts in two major pain-related regions, the dorsal root ganglion (DRG) and spinal cord dorsal horn. ⋯ Behavioral study showed that intrathecal mTOR inhibitor, rapamycin, did not affect acute nocicepetive transmission. The results indicate that although mTOR, p70S6K, and 4E-BP1 are highly expressed in the DRG and dorsal horn, their activate forms are very low in both regions under normal conditions. Our findings support the view that mTOR and its downstream effectors do not play a key role in acute pain.