Neuroscience
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The widespread application of ionizing radiation in industrial and medical fields leads to the increased brain exposure to X-rays. Radiation brain injury (RBI) seriously affects health of patients by causing cognitive dysfunction and neuroinflammation. However, the link between X-ray exposure and depressive symptoms and their detailed underlying mechanisms have not been well studied. ⋯ Moreover, X-ray exposure increased the expression of HMGB1, activated NLRP3 inflammasome signaling pathway and microglial cells, and then facilitated the release of pro-inflammatory cytokines, resulting in the pyroptosis and neuron loss both in vivo and in vitro. Additionally, glycyrrhizin (Gly), which is a HMGB1 inhibitor, reversed X-ray-induced behavioral changes and neuronal damage. Our findings indicated that HMGB1-mediated pyroptosis was involved in radiation-induced depression.
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Prenatal hypoxia (PH) is one of the most common adverse stimulation during pregnancy. The brain is fragile in the fetal period and sensitive to hypoxia. The offspring who have experienced PH may be at increased risk of developing neurodevelopmental disorders after birth and various neuropsychiatric diseases after adulthood. ⋯ The expression of the oxygen-sensitive subunit of hypoxia-inducible factor (Hif-1α) was significantly elevated, whereas Ten-eleven translocated methylcytosine dioxygenase 1 (Tet1) and c-Myc, which is closely related to cell proliferation, were significantly decreased in the hippocampus of the male offspring in the PH group. In addition, the PH group showed increased binding of Hif-1α to Tet1, and decreased binding of Tet1 to c-Myc, resulting in increased ubiquitinated degradation of c-Myc and decreased neurogenesis in the hippocampus of the male offspring. These findings suggest that Hif-1α regulates Tet1-c-Myc binding involved in depression-like behavior in PH offspring and Hif-1α can be used as a detection index of stress-related diseases.
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Affective disorders (i.e. anxiety and depression) are commonly observed in patients with epilepsy and induce seizure aggravation. Animal models of epilepsy that exhibit affective disorder features are essential in developing new neuromodulatory treatments. GEAS-W rats (Generalized Epilepsy with Absence Seizures, Wistar background) are an inbred model of generalized epilepsy showing spontaneous spike-wave discharges concomitant with immobility. ⋯ We observed a main effect of treatment and a significant treatment by strain interaction on anxiety-like and depressive-like behaviours, with active-tDCS GEAS-W rats entering the center of the open field more often and showing less immobility in the forced swimming test. Furthermore, there was a main effect of treatment on corticosterone with active-tDCS animals showing marked reduction in plasmatic levels. This study described preclinical evidence to support tDCS treatment of affective disorders in epilepsy and highlights corticosterone as a possible mechanism of action.
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Several event-related potentials (ERPs) are associated with the processing of valence-dependent augmented feedback during the practice of motor tasks. In this study, 38 students learned a sequential arm-movement-task with 192 trials in each of five practice sessions (960 practice trials in total), to examine practice-related changes in neural feedback processing. Electroencephalogram (EEG) was recorded in the first and last practice session. ⋯ A valence-independent increase of the P300 amplitude after practice might reflect an improved ability to update the internal representation based on feedback information. These results demonstrate that valence-dependent neural feedback processing changes with extensive practice of a novel motor task. Dissociating changes in latencies of different components support the assumption that they are related to distinct mechanisms of feedback-dependent learning.
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Brain EGR1 (early growth response protein 1) overexpression aggravates focal ischemic brain injury, but its role in intracerebral hemorrhage (ICH) induced cerebral injury remains obscure. In this study, a rat ICH model was established by injecting type VII collagenase into the brain, and EGR1 knockdown reversed the increase of hematoma area, neurological function score, brain water content, blood-brain barrier (BBB) permeability, inflammation, p300 and retinoid a X receptor-α (RXRα) protein levels, as well as RXRα acetylation level induced by ICH. EGR1 expression was up-regulated in primary brain microvascular endothelial cells (BMECs), neurons, and astrocytes after ICH induction, and the up-regulation was most significant in BMECs. ⋯ Furthermore, the STAT3/NF-κB pathway was activated after treatment with OGD plus hemin, which was suppressed by silencing EGR1. Treatment with Stattic (an inhibitor of STAT3) restrained the effect of OGD plus hemin on NF-κB pathway activity, inflammation, cell viability and TEER. In conclusion, EGR1 increased RXRα acetylation level by regulating p300, thereby aggravating brain damage in ICH rat model and dysfunction in BMECs, Through the STAT3/NF-κB pathway.