Neuroscience
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Recent studies have shown that the 5-HT1a receptor (5-HT1aR) in the central 5-HT (Serotonergic) system is involved in the pathophysiology of schizophrenia through its various receptors, and the dysfunction of the ventral hippocampus may be a key causative factor in schizophrenia. To date, whether the 5-HT1a receptor is involved in ventral hippocampal dysfunction and its internal mechanism remain unclear. In this study, schizophrenia-like animal model was induced by intraperitoneal injection of aspartate receptor antagonist MK-801 in male Sprague Dawley rats, and the role of 5-HT1aR in this animal model was investigated by bilaterally micro-infusing the 5-HT1aR antagonist WAY100635 into the ventral subiculum (vSub) of the hippocampus of rats. ⋯ Immunofluorescence analysis revealed that WAY100635 significantly increased the c-Fos expression in vSub. Western blot and immunohistochemical analysis showed that MK-801 induced up-regulation of 5-HT1aR and phospho-extracellular regulated protein kinase (p-ERK) pathway, while micro-infusion of the WAY100635 down-regulated 5-HT1aR and p-ERK in the vSub. Therefore, the results of the present study suggested that in vSub, the 5-HT1aR antagonist WAY100635 may attenuate MK-801-induced schizophrenia-like activity by modulating excitatory neurons and downregulating p-ERK.
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Alzheimer's disease is a fatal chronic neurodegenerative condition marked by a gradual decline in cognitive abilities and impaired vascular function within the central nervous system. This affliction initiates its insidious progression with the accumulation of two aberrant protein entities including Aβ plaques and neurofibrillary tangles. These chronic elements target distinct brain regions, steadily erasing the functionality of the hippocampus and triggering the erosion of memory and neuronal integrity. ⋯ These variations trigger neuronal malfunction and cognitive impairment. Intracellular tau accumulation in microglia and astrocytes triggers deleterious effects on the integrity of endothelium and cerebral blood supply resulting in further advancement of the ailment and cerebral instability. In this review, we will discuss the impact of tau on neurovascular impairment, mitochondrial dysfunction, oxidative stress, and the role of hyperphosphorylated tau in neuron excitotoxicity and inflammation.
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Randomized Controlled Trial
Alcohol drinking modified the effect of plasma YKL-40 levels on stroke-specific mortality of acute ischemic stroke.
Our study aimed to evaluate the association between plasma human cartilage glycoprotein-39 (YKL-40) and stroke-specific mortality at two years in acute ischemic stroke patients according to the drinking status and amount of alcohol consumption. We further investigated the effect of the interaction between these conditions and YKL-40 levels on the outcome. ⋯ gov; Unique identifier: NCT01840072.
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Previous studies on the chess game demonstrated that chess experts strongly rely on the activation of memory chunks to manifest accurate decision-making. Although the chunk memory might be affected by temporal constraints, it is unclear why the performance of chess experts is not significantly dropped under time pressure. In this study, our objective is to examine the variations in cognitive neural mechanisms between chess experts and novices under time pressure. ⋯ It was discovered that under temporal constraints, players exhibited different patterns of functional connectivity in frontal-parietal regions, suggesting that temporal stress can enhance segmentation processes in chess games. In particular, the experienced group exhibited significantly enhanced functional connectivity networks under time pressure including the dorsolateral prefrontal cortex, inferior frontal gyrus, supramarginal gyrus, and postcentral gyrus, which demonstrated the important role of the segmentation process for experienced players under time pressure. Our study found that experienced players were able to enhance recall, reorganize, and integrate chunks to improve chess performance under time pressure.