Neuroscience
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Abnormal spontaneous neural activity in children with growth hormone deficiency (GHD) has been found in previous resting-state functional magnetic resonance imaging (rs-fMRI) studies. Nevertheless, the spontaneous neural activity of GHD in different frequency bands is still unclear. Here, we combined rs-fMRI and regional homogeneity (ReHo) methods to analyze the spontaneous neural activity of 26 GHD children and 15 healthy controls (HCs) with age- and sex-matching in four frequency bands: slow-5 (0.014-0.031 Hz), slow-4 (0.031-0.081 Hz), slow-3 (0.081-0.224 Hz), and slow-2 (0.224-0.25 Hz). ⋯ In the slow-4 band, GHD children relative to HCs revealed increased ReHo in the right middle temporal gyrus, whereas reduced ReHo in the left superior parietal gyrus, right middle occipital gyrus, and bilateral medial parts of the superior frontal gyrus. In the slow-2 band, compared with HCs, GHD children showed increased ReHo in the right anterior cingulate gyrus, and several prefrontal regions, while decreased ReHo in the left middle occipital gyrus, and right fusiform gyrus and anterior cingulate gyrus. Our findings demonstrate that regional brain activity in GHD children exhibits extensive abnormalities, and these abnormalities are related to specific frequency bands, which may provide bases for understanding its pathophysiology significance.
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Patients with traumatic brain injury are typically maintained at low-normal levels of arterial partial pressure of carbon dioxide (PaCO2) to counteract the risk of elevated intracranial pressure during intensive care. However, several studies suggest that management at hypercarbic levels may have therapeutic benefit. Here we examined the impact of CO2 levels on spreading depolarizations (SD), a mechanism and marker of acute lesion development in stroke and brain trauma. ⋯ No differences in SD duration were observed. In both normoxia and hypoxia experiments, however, mean arterial pressures were negatively correlated with SD durations (normoxia R2 = -0.29; hypoxia R2 = -0.61, p's < 0.001). Our results suggest that any therapeutic benefit of elevated CO2 therapy may be dependent on an acidic shift in pH or may only be observed in conditions of focal brain injury.
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Spontaneously hypertensive rats (SHR) are the most common animal model used to study attention deficit hyperactivity disorder (ADHD). The purpose of this study was to look at the impact of neuroinflammation and autophagy on blood-brain barrier function in the prefrontal cortex and hippocampus of ADHD rats. The rats were separated into three groups: juvenile SHR (6 weeks), mature SHR (12 weeks), and comparable age WKY groups. ⋯ Moreover, autophagy of cells and the level of MMP2 and MPP9 in the prefrontal cortex and hippocampus increased in SHR rats. In addition, the expression of ZO-1 and occludin was decreased in SHR rats. To sum up, the increase of neuroinflammation and excessive autophagy were essential factors for the damage of blood-brain barrier structure and function.
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Astrocytes are implicated in stress-induced neuroinflammatory responses in depression. This paper was to explore the molecular mechanism of the E3 ubiquitin ligase NEDD4L (NEDD4 like E3 ubiquitin protein ligase) in depressed mice by regulating astrocyte activation, and to find a new target for depression. A mouse model of depression was established by CUMS (chronic mild unpredictable stress) in 48 6-week male C57BL/6 mice and injected with sh-NEDD4L vector for testing behavioral and cognitive abilities, histopathological changes, and the number of GFAP-positive cells. ⋯ NEDD4L inhibition increased GFAP-positive cells, increased PAX6 protein levels and decreased P2X7R mRNA and protein levels, and decreased inflammatory factor secretion in brain tissue and in vitro cells. PAX6 knockdown or P2X7R overexpression partially reversed the effects of NEDD4L inhibition on astrocyte activation and neuroinflammation. To conclude, highly-expressed NEDD4L in depression-like mouse brain inhibits astrocyte activation and exacerbates neuroinflammation by ubiquitinating PAX6 and promoting P2X7R level.
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The present study is designed to investigate the role of vagus nerve in the treatments of irritable bowel syndrome (IBS) and the associated central nervous system disorders. ⋯ The intestinal abnormalities and depressive symptoms in IBS rats can be improved by VNS treatment. This positive effect of VNS was achieved through α7nAChR-mediated inflammatory pathway and may also be associated with the decreased of BBB permeability.