Neuroreport最新文献

This study aimed to investigate the alteration of brain function based on resting-state functional MRI in patients after heat stroke. This study included 10 cases of patients after heat stroke and 10 cases of healthy controls. Abnormal brain function was calculated using amplitude of low-frequency fluctuations (ALFF) and degree centrality analysis, as well as functional connectivity analysis based on regions of interest (ROI). Correlation analyses were performed to evaluate the association between brain function changes and clinical scales. Combining ALFF and degree centrality results, the decreased brain regions included the left cuneus and the right angular gyrus, while the increased brain regions included the right cerebellar_Crus1. Using the left cuneus with significant differences in ALFF and degree centrality as ROI, the functional connectivity results revealed decreased brain regions including bilateral lingual gyrus, bilateral postcentral cingulate gyrus, and left precentral gyrus. The degree centrality value of the right cerebellar_Crus1 was positively correlated with glasgow coma scale (GCS) scores ( r  = 0.726, P  = 0.027), and the functional connectivity value of the right posterior cingulate gyrus was positively correlated with GCS scores ( r  = 0.717, P  = 0.030). Heat stroke patients exhibit abnormal activity in multiple brain regions, which has important clinical significance for evaluating the severity of the disease.

This study aims to investigate the effect of adipose-derived stem cells (ADSCs) transplantation on progranulin (PGRN) expression and functional recovery in rats with spinal cord injury (SCI). ADSCs were isolated from the inguinal adipose tissue of rats. A SCI model was created, and ADSCs were injected into the injured area. Various techniques were used to assess the effects of ADSCs transplantation, including hematoxylin-eosin staining, Masson staining, immunofluorescence staining, electron microscopy, MRI, and motor function assessment. The potential mechanisms of ADSC transplantation were investigated using gene expression analysis and protein analysis. Finally, the safety of this therapy was evaluated through hematoxylin-eosin staining and indicators of liver and kidney damage in serum. PGRN expression increased in the injured spinal cord, and ADSCs transplantation further enhanced PGRN levels. The group that received ADSCs transplantation showed reduced inflammation, decreased scar formation, increased nerve regeneration, and faster recovery of bladder function. Importantly, motor function significantly improved in the ADSC transplantation group. ADSCs transplantation enhances functional regeneration in SCI by upregulating PGRN expression, reducing inflammation and scar formation, and promoting nerve regeneration and myelin repair. These findings suggest that ADSC transplantation is a potential therapy for SCI.

Much behavioral research has revealed interactive effects between stimulus quality and semantic priming in visual word recognition, practically in favor of the interactive activation model. However, the limited number of event-related brain potential (ERP) studies have yielded inconsistent results considering this interaction's impact on N400 amplitude. The current ERP study aimed to examine whether the joint effects of stimulus quality and semantic priming were specific to the lexical decision task. We used both behavioral measures and ERP recordings to evaluate the joint effects of stimulus degradation (i.e. highly vs. slightly degraded) and semantic priming (i.e. semantically related vs. unrelated) in a lexical decision task involving visual recognition of Chinese characters. The results showed significant degradation-by-priming interactions on response times and N400 amplitude ( P  < 0.05), with larger semantic priming effects on slightly degraded targets. These converging behavioral and electrophysiological findings provide evidence in accordance with the interactive activation models of visual word recognition, in which the early-stage visual processing (i.e. degradation) cascades into the later-stage semantic processing (i.e. priming), thus yielding interactions observed in N400 amplitude.

The blood-brain barrier (BBB) strictly limits the entry of most exogenous therapeutic drugs into the brain, which brings great challenges to the drug treatment of refractory central diseases, including the treatment of ischemic stroke. Our previous studies have shown that specific mode electroacupuncture stimulation (SMES) can temporarily open the BBB, but with the mechanisms largely unknown. This study explored whether SMES opens the BBB in the infarcted border zone of rats during middle cerebral artery occlusion/reperfusion recovery, and whether this is related to p65 or vascular endothelial growth factor A (VEGFA) modulation of tight junction protein expression through in vivo and in vitro studies. Evans blue, FITC-dextran, mouse-derived nerve growth factor (NGF), and transendothelial electrical resistance values were used to evaluate the permeability of the BBB. Additionally, microvascular endothelial cells and astrocytes were utilized for in vitro study. Immunofluorescence, immunohistochemistry, western blot, and ELISA were employed to assess related protein expression. SMES significantly increased vascular permeability for Evans blue and NGF in the infarcted border zone, and increased the expression of VEGFA by activating p-p65, thereby reducing the expression of tight junction proteins Occludin and ZO-1. Correspondingly, oxygen glucose deprivation/reoxygenation activated p-p65 in and induced VEGFA secretion from astrocytes in vitro. Their conditioned medium reduced the expression of Occludin in bEnd.3 cells and increased the permeability of FITC-dextran. The mechanism of SMES opening infarcted border zone BBB is partly related to its actions on p65, VEGFA, and tight junction proteins.

Even though considerable progress has been made to reduce insult, ischemic stroke is still a significant cause of mortality and morbidity in the world, and new therapeutic strategies are urgently needed. In the present study, the magnesium salt of salvianolic acid B (SalB) and ginsenoside Rg1 (Rg1) combination as a multicomponent strategy against stroke was evaluated. The synergistic effect of Sa1B and Rg1 was evaluated by Bliss independence analysis on the middle cerebral artery occlusion model. The infarct volume, neuroethology, cerebral structure, and neurocyte number were evaluated by 3,5-triphenyltetrazolium chloride staining, Longa score, Garcia score, hematoxylin-eosin staining, and Nissl staining, respectively. Metabolomics was used to search for potential biomarkers and explore the mechanism of Sa1B/Rg1. First, the superior effects of SalB/Rg1 than SalB or Rg1 at the same dose were evaluated. Compared with SalB ( P  < 0.001) or Rg1 ( P  < 0.01), SalB/Rg1 significantly decreased infarct volume through 3,5-triphenyltetrazolium chloride staining and protected the structural integrity of cortex and striatum. The superior effect of SalB/Rg1 on neurological behavior was also detected compared with SalB or Rg1 significantly. Accompanying behavioral improvement, a considerable increase of SalB/Rg1 on neurons detected by Nissl staining was found on the cortex compared with SalB ( P  < 0.05) or Rg1 ( P  < 0.01). Second, the synergistic effect between SalB and Rg1 was strictly verified by Bliss independence analysis ( P  < 0.01) based on infarct volume. Finally, alleviation of cerebral metabolic disorders may be the possible mechanism of SalB/Rg1. Our study provided a multicomponent strategy against ischemic stroke, with not only dose reduction but also improved efficacy relative to single agents.

Aging generally affects food consumption and energy metabolism. Since the feeding center is located in the hypothalamus, it is a major target for understanding the mechanism of age-related changes in eating behavior and metabolism. To obtain insight into the age-related changes in gene expression in the hypothalamus, we investigated genes whose expression changes with age in the hypothalamus. A DNA microanalysis was performed using hypothalamus samples obtained from young (aged 24 weeks) and old male mice (aged 138 weeks). Gene Ontology (GO) analysis was performed using the identified differentially expressed genes. We observed that the expression of 377 probe sets was significantly altered with aging (177 were upregulated and 200 were downregulated in old mice). As a result of the GO analysis of these probe sets, 16 GO terms, including the neuropeptide signaling pathway, were obtained. Intriguingly, although the food intake in old mice was lower than that in young mice, we found that several neuropeptide genes, such as agouti-related neuropeptide ( Agrp ), neuropeptide Y ( Npy ), and pro-melanin-concentrating hormone ( Pmch ), all of which promote food intake, were upregulated in old mice. In conclusion, this suggests that the gene expression pattern in the hypothalamus is regulated to promote food intake.

Dysregulated appetite is common in autism spectrum disorder (ASD) and it includes excessive interest in tasty foods. Overconsumption of palatable fluids has been found in the valproic acid-induced ASD rat. Though ASD has a strong genetic component, the link between ASD-related genes and appetite for palatable foods remains elusive. We focused on the CNTNAP2 gene whose deletion in mice recapitulates human ASD symptoms. We investigated whether Cntnap2-/- male mice consume greater amounts of palatable 10% sucrose, 0.1% saccharin, and 4.1% intralipid solutions offered in episodic meals either in a no-choice paradigm or a two-bottle choice test. We examined how sucrose intake affects c-Fos immunoreactivity in feeding-related brain areas. Finally, we determined doses at which intraperitoneal oxytocin decreases sucrose intake in mutants. In the single-bottle tests, Cntnap2-/- mice drank more sucrose, saccharin, and intralipid compared to WTs. Given a choice between two tastants, Cntnap2-/- mice had a higher preference for sucrose than intralipid. While the standard 1 mg/kg oxytocin dose reduced sucrose intake in WTs, a low oxytocin dose (0.1 mg/kg) decreased sucrose intake in Cntnap2-/- mice. Sucrose intake induced a more robust c-Fos response in wild-type (WT) than Cntnap2-/- mice in the reward and hypothalamic sites and it increased the percentage of Fos-immunoreactivity oxytocin neurons in WTs, but not in mutants. We conclude that Cntnap2-/- mice overconsume palatable solutions, especially sucrose, beyond levels seen in WTs. This excessive consumption is associated with blunted c-Fos immunoreactivity in feeding-related brain sites, and it can be reversed by low-dose oxytocin.

Previous studies have found alterations in the local regional homogeneity of brain activity in individuals diagnosed with major depressive disorder. However, many studies have failed to consider that even during resting states, brain activity is dynamic and time-varying. The lack of investigation into the dynamic regional homogeneity has hindered the discovery of biomarkers for depression. This study aimed to assess the utility of the dynamic regional homogeneity by a machine learning model (support vector machine). Sixty-five individuals with dynamic regional homogeneity and 57 healthy controls participated in resting-state functional magnetic resonance rescanning and scale estimating. The dynamic regional homogeneity and receiver operating characteristic curve methods were used for analysis of the imaging data. Relative to healthy controls, major depressive disorder patients displayed increased dynamic regional homogeneity values in the left precuneus and right postcentral gyrus. Additionally, receiver operating characteristic curve results of the dynamic regional homogeneity values in the left precuneus and right postcentral gyrus could distinguish major depressive disorder patients from healthy controls; furthermore, changes in the dynamic regional homogeneity were correlated with depression severity.

This study aimed to compare the effect of the early postmenopausal period on resting-state electroencephalographic spectral power with that of the premenopausal period and to analyze the correlation between electroencephalographic spectral power values and endogenous ovarian hormone levels. This study involved 13 early postmenopausal women and 10 premenopausal women in the early follicular, 10 in the ovulatory phase, and 10 in the early luteal phase who underwent resting-state quantitative electroencephalographic spectral power with eyes closed and endogenous ovarian hormone measurements. The delta, theta, alpha1, alpha2, beta1, and beta2 absolute power were compared between the early postmenopausal and premenopausal groups. Correlations between electroencephalographic spectral power values and 17β estradiol, progesterone, follicle-stimulating hormone (FSH), and luteinizing hormone levels were analyzed in early postmenopausal women. Compared with the premenopausal group, the early postmenopausal group showed significantly higher resting-state theta power in the frontal region, alpha1 and alpha2 power in the frontal and central regions, beta1 power in the frontal, central, parietal, and occipital regions, and beta2 power in the centroparietal region. Beta2 power values were positively correlated with FSH levels. The current findings highlight that early postmenopausal women show greater resting-state alpha and beta power, which suggests cortical excitability of fast frequency bands involved in states of alertness, focus of attention, cognition, and emotion. Additionally, we emphasized the effect of FSH levels on fast cortical activation in early postmenopausal women.

Thiamine deficiency is a well-known risk factor for the development of severe encephalopathy, such as Wernicke encephalopathy and Korsakoff syndrome, but the underlying mechanism is still mysterious. This study aims to investigate the expression levels of thiamine metabolism genes in different tissues and their impact on brain susceptibility to thiamine deficiency. The mRNA and protein levels of four genes known to be associated with thiamine metabolism: thiamine pyrophosphokinase-1 ( Tpk ), Solute carrier family 19 member 2 ( Slc19a2 ), Slc19a3 , and Slc25a19 , in the brain, kidney, and liver of mice were examined. Thiamine diphosphate (TDP) levels were measured in these tissues. Mice were subjected to dietary thiamine deprivation plus pyrithiamine (PTD), a specific TPK inhibitor, or pyrithiamine alone to observe the reduction in TDP and associated pathological changes. TPK mRNA and protein expression levels were lowest in the brain compared to the kidney and liver. Correspondingly, TDP levels were also lowest in the brain. Mice treated with PTD or pyrithiamine alone showed an initial reduction in brain TDP levels, followed by reductions in the liver and kidney. PTD treatment caused significant neuron loss, neuroinflammation, and blood-brain barrier disruption, whereas dietary thiamine deprivation alone did not. TPK expression level is the best indicator of thiamine metabolism status. Low TPK expression in the brain appears likely to contribute to brain susceptibility to thiamine deficiency, underscoring a critical role of TPK in maintaining cerebral thiamine metabolism and preventing thiamine deficiency-related brain lesions.