Neuroscience
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The relationship between attention and incentive motivation has been mostly examined by administering Posner style cueing tasks in humans and varying monetary stakes. These studies found that higher incentives improved performance independently of spatial attention. However, the ability of the cueing task to measure actual attentional orienting has been debated by several groups that have highlighted the function of the motor system in affecting the behavioral features that are commonly attributed to spatial attention. ⋯ In Experiment 2, the task was modified to fit a paradigm of Go/NoGo target identification. We found that attention and motivation interacted exclusively in Experiment 2, wherein anticipated motor activation was discouraged and more demanding visual processing was imposed. Consequently, we suggest a protocol that provides novel insights into the study of the relationship between spatial attention and motivation and highlights the influence of the arm motor system in the estimation of the deployment of spatial attention.
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Myeloid-derived suppressor cells (MDSCs) have strong immunosuppressive characteristics, which allow them to limit inflammation and facilitate wound healing and recovery. Although MDSCs are a newly-determined cell type that is gaining attention in the immunology field, their neuroimmunological characteristics remain unstudied. ⋯ MDSCs are among the first responders to tissue injury, responding even prior to microglial activation. Positron emission tomography imaging of translocator protein results suggest that infiltrating MDSCs suppress neuronal inflammation and interact with resident immune cells, like microglia, following focal TBI.
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The adverse consequences of early-life sleep deprivation on mental health are well recognized, yet many aspects remain unknown, therefore, animal studies can offer useful insights. Male Sprague-Dawley rats at postnatal day (PND) 19 were subjected to sleep deprivation (SD) for 14 days (6-8 hours/day). Control (CON) rats were gently handled. ⋯ Our postulation is that SD by increasing PFC oxido-inflammation, negatively affects glutamate receptor subunits and PSD95 expression, which disrupts synapse formation and maturation, potentially causing anxiety-like behavior at PND33. Oxido-inflammation further results in MKP-1 and CaMKII-mediated blockade of ERK1/2 activation, which inhibits CREB dependent BDNF expression. This most likely disrupts neuronal circuit development, leading to depression-like behavior at PND90.
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The article studies the effect of melatonin on the intensity of free radical oxidation, the functioning of the enzymatic components of the antioxidant system and their transcriptional regulation in rats with experimental cerebral ischemia/reperfusion of the brain. The development of ischemia/reperfusion was characterized by the activation of apoptotic processes and the accumulation of mRNA of the genes Sod1, Cat, Gpx1, Gsr, Hif-1α, Nrf2, Nfkb2, and Foxo1 in the rats' brains. ⋯ At the same time, there was a shift in the activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, which increased in the presence of a pathology, towards the control values. The revealed changes may be accounted for by antioxidant and neuroprotective properties of melatonin, which provided a decrease in the degree of mobilization of the protective systems in animal organism.
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The over-activation of N-methyl-D-aspartate receptors (NMDARs) is the main cause of neuronal death in brain ischemia. Both the NMDAR and the Acid-sensing ion channel 1a (ASIC1a) are present in the postsynaptic membrane of the central nervous system (CNS) and participate in physiological and pathological processes. However, the specific role played by ASIC1a in these processes remains elusive. ⋯ Furthermore, brain infarct sizes were reduced by a greater degree in older mice compared to younger ones when ASIC1a activity was suppressed. These data suggest that ASIC1a activity selectively enhances the function of triheteromeric NMDARs and exacerbates ischemic neuronal death especially in older animal brains. We propose ASIC1a as a novel therapeutic target for preventing and reducing the detrimental effect of brain ischemia in humans.