Brain Research最新文献

{"title":"Arsenic-induced mice model of Parkinson’s disease: Revealing the neurotoxicity of arsenic through mitochondrial complexes inhibition and dopaminergic neurodegeneration in the substantia nigra region of brain","authors":"Ankumoni Dutta ,&nbsp;Rubina Roy ,&nbsp;Mritunjay Pandey ,&nbsp;Sushila Chhetry ,&nbsp;Banashree Chetia Phukan ,&nbsp;Abhideep Roy ,&nbsp;Pallab Bhattacharya ,&nbsp;Anupom Borah","doi":"10.1016/j.brainres.2025.149493","DOIUrl":"10.1016/j.brainres.2025.149493","url":null,"abstract":"<div><div>The role of environmental contaminants in causing Parkinson’s disease (PD) is well known, with rotenone and paraquat being the notable neurotoxins. Traces of the metalloid arsenic are frequently found in drinking water which is considered a threat to the brain’s health. Pre-clinical and epidemiological studies have associated arsenic with PD whereby behavioral and neurochemical alterations were observed. However, the impact of arsenic toxicity on the dopaminergic neurons of substantia nigra (SN), the hallmark region which degenerates in PD, has not been shown yet. In the present study, administration of 20 mg/kg b.w., arsenic for 28 days caused significant loss of dopaminergic neurons and their terminals respectively in the SN and striatum regions of mice brain. Moreover, the arsenic-fed rodents exhibited depleted striatal dopamine, prolonged latency to move and correct posture, and reduced exploratory behavior and neurological severity. Further, mitochondrial complexes II and IV were found to be inhibited in the SN, cortex, striatum, and hippocampus of arsenic-fed mice. Additionally, inflammatory marker glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) expressed in glial cells and neurons respectively were enhanced in the nigrostriatal pathway of arsenic-fed animals. The present study for the first time reports that arsenic causes Parkinsonism by degenerating nigrostriatal dopaminergic neurons through mitochondrial complex inhibition and inflammatory stress. The study further puts forward validatory evidence for the potential of arsenic in causing PD and the reliability of the arsenic-induced PD model for exploring the disease pathogenesis and treatment.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149493"},"PeriodicalIF":2.7,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of noradrenergic signalling reverses stress-induced changes in the hippocampus: Involvement of orexinergic systems","authors":"Masoumeh Sarfi,&nbsp;Mahmoud Elahdadi Salmani,&nbsp;Taghi Lashkarbolouki,&nbsp;Iran Goudarzi","doi":"10.1016/j.brainres.2025.149491","DOIUrl":"10.1016/j.brainres.2025.149491","url":null,"abstract":"<div><div>Stress can be beneficial for adapting to dangerous situations in the short term but can be damaging in the long term, especially in the hippocampus. The noradrenergic and orexinergic systems play important roles in stress response. This study investigated the effect of noradrenergic activation on changes induced by chronic stress in the hippocampus and the involvement of orexinergic modulation in this process.</div><div>This study examined five groups of 40 male Wistar rats (4 + 4 animals/ group): control, chronic stress, acute stress, control with noradrenergic activation, and chronic stress with noradrenergic activation. Hippocampal tissue and blood plasma were the primary specimens analyzed. The researchers measured plasma corticosterone (CORT) using a fluorometric method, examined the expression of prepro-orexin (prepro-OX), orexin receptor-1 (OXr1), and glucocorticoid receptor (GR) through RT-PCR, and quantified neuronal populations using Nissl staining.</div><div>Acute and chronic stress increased plasma CORT levels and gene expression of prepro-OX, OXr1, and GR, while decreasing neuronal numbers, with chronic stress having a more pronounced effect. Yohimbine-treated and/or stressed rats exhibited elevated plasma CORT levels. Chronic stress substantially upregulated GR and increased prepro-OX and OXr1 expressions whereas yohimbine recovered those profiles in chronically stressed animals. Conversely, chronic stress reduced hippocampal neuronal populations, and chronic stress combined with yohimbine partially compensated for the neuronal numbers compared to chronic stress alone.</div><div>These results suggest that noradrenergic signalling can reverse chronic stress-induced impairments in prepro-OX, OXr1 and GR expressions, and neuronal populations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149491"},"PeriodicalIF":2.7,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced electroencephalogram signal classification: A hybrid convolutional neural network with attention-based feature selection","authors":"Bao Liu ,&nbsp;Yuxin Wang ,&nbsp;Lei Gao ,&nbsp;Zhenxin Cai","doi":"10.1016/j.brainres.2025.149484","DOIUrl":"10.1016/j.brainres.2025.149484","url":null,"abstract":"<div><div>Accurate recognition and classification of motor imagery electroencephalogram (MI-EEG) signals are crucial for the successful implementation of brain-computer interfaces (BCI). However, inherent characteristics in original MI-EEG signals, such as nonlinearity, low signal-to-noise ratios, and large individual variations, present significant challenges for MI-EEG classification using traditional machine learning methods.</div><div>To address these challenges, we propose an automatic feature extraction method rooted in deep learning for MI-EEG classification. First, original MI-EEG signals undergo noise reduction through discrete wavelet transform and common average reference. To reflect the regularity and specificity of brain neural activities, a convolutional neural network (CNN) is used to extract the time-domain features of MI-EEG. We also extracted spatial features to reflect the activity relationships and connection states of the brain in different regions. This process yields time series containing spatial information, focusing on enhancing crucial feature sequences through talking-heads attention. Finally, more abstract spatial–temporal features are extracted using a temporal convolutional network (TCN), and classification is done through a fully connected layer. Validation experiments based on the BCI Competition IV-2a dataset show that the enhanced EEG model achieves an impressive average classification accuracy of 85.53% for each subject. Compared with CNN, EEGNet, CNN-LSTM and EEG-TCNet, the classification accuracy of this model is improved by 11.24%, 6.90%, 11.18% and 6.13%, respectively. Our work underscores the potential of the proposed model to enhance intention recognition in MI-EEG significantly.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149484"},"PeriodicalIF":2.7,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoparticle-enhanced delivery of resveratrol for targeted therapy of glioblastoma: Modulating the Akt/GSK-3β/NF-kB pathway in C6 glioma cells","authors":"Gurpreet Singh ,&nbsp;Paras Famta ,&nbsp;Saurabh Shah ,&nbsp;Ganesh Vambhurkar ,&nbsp;Giriraj Pandey ,&nbsp;Rahul Kumar ,&nbsp;Prakash Kumar ,&nbsp;Atul Mourya ,&nbsp;Jitender Madan ,&nbsp;Saurabh Srivastava ,&nbsp;Dharmendra Kumar Khatri","doi":"10.1016/j.brainres.2024.149411","DOIUrl":"10.1016/j.brainres.2024.149411","url":null,"abstract":"<div><h3>Objective</h3><div>The study aims to explore Resveratrol (RES) as a potential therapeutic agent for Glioblastoma multiforme (GBM), a challenging brain cancer. RES, a polyphenolic compound with known benefits in various diseases including cancer, has shown promise in inhibiting glioma progression through its effects on the AKT signaling pathways. However, its limited ability to cross the blood–brain barrier restricts its clinical application in GBM treatment. This study seeks to enhance efficacy of RES by developing RES-loaded nanoparticles designed to improve penetration into glioma cells and potentially overcome the blood–brain barrier, thereby enhancing therapeutic outcomes.</div></div><div><h3>Methods</h3><div>Albumin nanoparticles were prepared and characterized using FT-IR, X-RD, and SEM to determine particle size. <em>In vitro</em> experiments were conducted using the C6 glioma cell line, employing MTT assays, Immunofluorescence, DC-FDA staining, and western blot analysis. Molecular docking studies were also performed to assess ability of RES to inhibit the AKT/GSK-3β/NF-kB pathway.</div></div><div><h3>Results</h3><div><em>In vitro</em> results demonstrated that RES-loaded nanoparticles induced apoptosis and reduced proliferation of C6 glioma cells compared to controls. Molecular docking studies confirmed RES’s potential as an inhibitor targeting the AKT/GSK-3β/NF-kB pathway. Western blot analysis revealed downregulation of AKT and GSK-3β expression in cells treated with RES-loaded nanoparticles, accompanied by increased caspase 1 levels and decreased bcl2 expression, indicative of apoptosis.</div></div><div><h3>Conclusion</h3><div>The findings suggest that RES effectively targets the AKT/GSK-3β/NF-kB signaling pathway in glioma cells. Furthermore, RES-loaded albumin nanoparticles significantly enhance therapeutic efficacy by improving cellular penetration, highlighting their potential in advancing GBM treatment strategies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149411"},"PeriodicalIF":2.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revealing shared molecular drivers of brain metastases from distinct primary tumors","authors":"Carlos Alberto de Carvalho Fraga ,&nbsp;Leandro Tiburske ,&nbsp;Gabriel Victor Lucena da Silva ,&nbsp;Adriana Simizo ,&nbsp;Mauro Cesar Cafundó de Morais ,&nbsp;Ana Kelly da Silva Fernandes Duarte ,&nbsp;Henry David Mogollón García ,&nbsp;Thiago Dominguez Crespo Hirata ,&nbsp;Helder I. Nakaya","doi":"10.1016/j.brainres.2025.149456","DOIUrl":"10.1016/j.brainres.2025.149456","url":null,"abstract":"<div><div>Brain metastasis is the most common type of brain cancer, associated with significant neurological dysfunction and a poor prognosis. We investigated the transcriptome of 128,421 single-cells of 36 brain metastases, originating from a variety of primary tumors, including melanoma, breast, lung, ovarian, colorectal, and renal cancers. Our aim was to identify common molecular factors across these tumors, shedding light on key interactions that facilitate tumor establishment in the brain. We specifically focused on the dynamics of the blood-tumor barrier and its effects on endothelial cells, pericytes, and astrocytes. Our analysis decoded complex cell–cell communications, emphasizing the crucial role of astrocytes in the tumor microenvironment (TME). This provided insights into how these interactions impact the permeability of the blood-tumor barrier and contribute to the development of brain metastases. We identified the VEGFA, SEMA3, and SPP1 pathways as key regulators in brain metastasis, affecting vascular permeability and cellular dynamics. Spatial transcriptome analysis confirmed our findings and linked these pathways to TME enrichment. The pronounced expression of VEGFA by cancer cells suggests a significant activation of angiogenic pathways, influencing vascular responses and the intricate architecture of brain tissue. The interplay of these signaling pathways underlines the complexity of molecular interactions that define the microenvironment of brain metastases.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149456"},"PeriodicalIF":2.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct contributions of BDNF/MEK/ERK1/2 signaling pathway components to whisker-dependent tactile learning and memory","authors":"Hitomi Soumiya,&nbsp;Shingo Mori,&nbsp;Kohta Kageyama,&nbsp;Masateru Kawakami,&nbsp;Aoi Nara,&nbsp;Shoei Furukawa,&nbsp;Hidefumi Fukumitsu","doi":"10.1016/j.brainres.2024.149404","DOIUrl":"10.1016/j.brainres.2024.149404","url":null,"abstract":"<div><div>Whisker-mediated tactile perception is essential for rodent navigation, food acquisition, and social interactions. However, the molecular mechanisms underlying tactile information processing, learning, and memory have not been studied to the same extent as for other modalities. Using immunohistochemical staining, we investigated changes in regional c-Fos expression as an index of neuronal activity and phosphorylated (p)ERK1/2 as an index of ERK1/2 activity in mice trained on a tactile-cued 8-arm radial maze task. Over 12 trials, mice learned to selectively explore four baited arms covered with wire as the tactile cue while avoiding un-baited uncovered arms. The density of c-Fos⁺ cells was significantly higher in somatosensory cortex but not frontal cortex or amygdala of mice exposed to tactile cue – bait pairing compared to mice exposed to the same maze with all arms baited with or without tactile cues (unpaired conditions). The density of pERK1/2⁺ cells was also increased after paired trials 7 and 12 but not after paired trials 1 and 3 in frontal cortex, amygdala, and somatosensory cortex compared to mice exposed to the unpaired condition. The MEK1/2 inhibitor SL327 reduced c-Fos expression in frontal cortex and amygdala when applied during early trials, but impaired working memory when applied before later trials without affecting c-Fos expression. Heterozygous BDNF knockout mice exhibited impaired task learning and reduced pERK1/2 expression in frontal cortex and amygdala but not somatosensory cortex. These findings suggest that the BDNF/MEK/ERK1/2 pathway selectively promotes memory trace formation in frontal cortex and amygdala but not encoding in somatosensory cortex.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149404"},"PeriodicalIF":2.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential molecular mechanisms of tobacco smoke exposure in Alzheimer’s disease","authors":"Yunqi Xie ,&nbsp;Mingxue Yang ,&nbsp;Haochen Wang,&nbsp;Yuting Chen,&nbsp;Xiaobo Shi,&nbsp;Huanwen Tang,&nbsp;Qian Sun","doi":"10.1016/j.brainres.2024.149394","DOIUrl":"10.1016/j.brainres.2024.149394","url":null,"abstract":"<div><h3>Background</h3><div>Smoking is detrimental to health, with tobacco use being a critical factor in the development of various neurodegenerative diseases, including Alzheimer’s disease (AD), which progressively impairs brain function and poses a significant threat to public health. This study aims to examine the potential genetic alterations induced by smoking that are associated with AD and to investigate the underlying regulatory mechanisms. The research will provide theoretical foundations for targeted prevention and treatment strategies for AD.</div></div><div><h3>Methods</h3><div>This study analyzed datasets from the Gene Expression Omnibus (GEO) and the Comparative Toxicogenomics Database (CTD) to identify genes affected by tobacco smoke exposure and those altered in patients with AD relative to normal controls. We conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses using OmicShare tools to screen for key pathways. Key genes were identified by constructing protein–protein interaction networks (PPI) in the STRING database with the aid of CytoHubba. Additionally, the binding activity of the proteins encoded by these key genes to nicotine, the main component of tobacco, was analyzed using molecular docking techniques. Finally, the analytical results were verified using Quantitative Real-Time Polymerase Chain Reaction.</div></div><div><h3>Results</h3><div>The CTD identified 12,164 CE-related genes affected by tobacco smoke exposure. A comparison of these datasets yielded 94 common genes that were both influenced by tobacco and differentially expressed across all brain regions. The GO and KEGG pathway enrichment analyses showed that these common differentially expressed genes (DEGs) were predominantly enriched in the Wnt/β-catenin and PI3K-AKT signaling pathways. The DEGs’ PPI network, constructed using the STRING database, highlighted key genes such as HSP90AB1, SOS2, MAGI1, and YWHAZ. Molecular docking studies demonstrated that nicotine binds effectively to the protein structures of these key genes, primarily through amino acid residues such as Ser and Glu. Experimental validation showed that HSP90AB1 and YWHAZ exhibited notable expression discrepancies under varying concentrations of cigarette smoke extract (CSE) treatments, particularly demonstrating a pronounced down-regulation trend at elevated concentrations.</div></div><div><h3>Conclusion</h3><div>The study indicates that tobacco may impact the function of transmembrane transporter proteins and contribute to the development of AD by affecting key genes such as HSP90AB1 and YWHAZ, as well as signaling pathways like PI3K-AKT.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149394"},"PeriodicalIF":2.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142851944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of dexmedetomidine in postoperative cognitive dysfunction and sleep improvement in aged rats by regulating the PI3K/Akt signaling pathway and its mechanism","authors":"Ying Kong ,&nbsp;Xiaopeng Wang ,&nbsp;Jun Pang ,&nbsp;Haiyan Huo ,&nbsp;Xiaofang Wang","doi":"10.1016/j.brainres.2025.149482","DOIUrl":"10.1016/j.brainres.2025.149482","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to explore the mechanism of dexmedetomidine (Dex) in improving postoperative cognitive dysfunction (POCD) and postoperative sleep in aged rats through the PI3K/Akt signaling pathway.</div></div><div><h3>Methods</h3><div>Splenectomy was used to establish a POCD model in aged rats. Open field test (OFT) and new object recognition test (NORT) were used to observe the cognitive function of rats The awakening and sleep times of rats were recorded. Hematoxylin-eosin, Nissl, and TUNEL staining were adopted to examine histopathological alterations, neuronal cell damage, and apoptosis, respectively; western blot to detect the activation of the PI3K/Akt signaling pathway and the protein level of apoptosis factors Bcl-2, Bax, and cleaved caspase-3; enzyme-linked immunosorbent assay to quantify the concentrations of inflammatory factors IL-6, IL-1β, and TNF-α.</div></div><div><h3>Results</h3><div>On days 1, 7, and 14 post-splenectomy surgery, aged rats exhibited shortened moving distance in OFT, reduced discrimination rate in NORT, prolonged awakening time, and shortened sleep time, while such effect was reversed by further Dex treatment. In addition, neuronal damage, inflammatory response, and apoptosis occurred in the hippocampal CA1 area in aged rats but can be attenuated by Dex treatment. Dex triggered the activation of the PI3K/Akt signaling pathway in the hippocampus in aged rats after surgery, and inhibition of the PI3K/Akt signaling pathway can result in a partial reversal of the alleviating effects observed with Dex treatment.</div></div><div><h3>Conclusion</h3><div>Dex improves POCD and postoperative sleep in aged rats by activating the PI3K/Akt signaling pathway to reduce inflammatory response and apoptosis in the hippocampal CA1 area.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1852 ","pages":"Article 149482"},"PeriodicalIF":2.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture promotes neural function recovery by alleviating mitochondria damage in cerebral ischemia mice","authors":"Feng Yashuo ,&nbsp;Guan Chong ,&nbsp;Yang Zhe ,&nbsp;Cao Lu ,&nbsp;Xie Hongyu ,&nbsp;Wu Yi ,&nbsp;Wang Nianhong","doi":"10.1016/j.brainres.2025.149479","DOIUrl":"10.1016/j.brainres.2025.149479","url":null,"abstract":"<div><h3>Aims</h3><div>This study aimed to observe the effect of electroacupuncture (EA) at Zusanli point (ST36) on motor function of cerebral ischemia mice, and to observe the effect of EA on mitochondrial morphology of <em>peri</em>-infarct cortex neurons in cerebral ischemia mice.</div></div><div><h3>Methods</h3><div>Middle cerebral artery occlusion (MCAO) was used to develop an ischemic stroke mice model. EA treatment was performed for three consecutive days for 15 min per day after MCAO modeling. We investigated the therapeutic effects of EA on MCAO mice by performing neurobehavioral assessment (modified Neurological Severity Score, Rotarod test, Open-field test and Gait analysis) and TTC staining. The morphology and function of neuronal mitochondria were evaluated by transmission electron microscopy, qRT-PCR, chemiluminescence, and western blot. Nissl staining, TUNEL staining and immunofluorescence staining were used to observe neuronal morphology and apoptosis. Furthermore, ELISA was employed to measure the expression levels of inflammatory factors in mouse serum.</div></div><div><h3>Results</h3><div>EA alleviated motor dysfunction and infarct volume in mice with cerebral ischemia. It improved the neuronal mitochondria damage in MCAO mice, and decreased the protein and mRNA expression level of mitochondrial fission related proteins (FIS1 and Drp1). In addition, EA can reduce neuronal damage and apoptosis of nerve cells, and decrease the level of inflammatory factors (IL-1β, TNF-α, IL-6 and IL-8) in cerebral ischemia mice.</div></div><div><h3>Conclusion</h3><div>EA therapy can improve motor dysfunction and alleviate the damage of neuron mitochondria in cerebral ischemic mice.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149479"},"PeriodicalIF":2.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Happy and angry facial expressions are processed independently of task demands and semantic context congruency in the first stages of vision – A mass univariate ERP analysis","authors":"Calla Mueller,&nbsp;Amie J. Durston,&nbsp;Roxane J. Itier","doi":"10.1016/j.brainres.2025.149481","DOIUrl":"10.1016/j.brainres.2025.149481","url":null,"abstract":"<div><div>Neural decoding of others’ facial expressions is critical in social interactions and has been investigated using scalp event related potentials (ERPs). However, the impact of task and emotional context congruency on this neural decoding is unclear. Previous ERP studies employed classic statistical analyses that only focused on specific electrodes and time points, which inflates type I and type II errors. The present study re-analyzed the study by Aguado et al. (2019) using robust data-driven Mass Univariate Statistics across every time point and electrode and rejected trials with early reaction times to rule out motor-related activity on neural recordings. Participants viewed neutral faces paired with negative or positive situational sentences (e.g. “She catches her partner cheating on her with her best friend”), followed by the same individuals’ faces expressing happiness or anger, such that the facial expressions were congruent or incongruent with the situation. Participants engaged in two tasks: an emotion discrimination task, and a situation-expression congruency discrimination task. We found significant effects of expression largest during the N170-P2 interval, and effects of congruency and task around an LPP-like component. However, the effect of congruency was significant only in the congruency task, suggesting a limited and task-dependant influence of semantic context. Importantly, emotion did not interact with any factor neurally, suggesting facial expressions were decoded automatically during the first 400 ms of vision, regardless of context congruency or task demands. The results and their discrepancies with the original findings are discussed in the context of ERP statistics and the replication crisis.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1851 ","pages":"Article 149481"},"PeriodicalIF":2.7,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}