Brain Research Bulletin最新文献

{"title":"Understanding autism: Causes, diagnosis, and advancing therapies","authors":"Min Wang ,&nbsp;Xiaozhuang Zhang ,&nbsp;Liyan Zhong ,&nbsp;Liqin Zeng ,&nbsp;Ling Li ,&nbsp;Paul Yao","doi":"10.1016/j.brainresbull.2025.111411","DOIUrl":"10.1016/j.brainresbull.2025.111411","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) is a neurodevelopmental condition marked by difficulties in social communication, languages, and repetitive behaviors. Its rising prevalence has made it a critical global public health issue. ASD is believed to arise from a combination of genetic and environmental influences. While some gene mutations associated with ASD have been identified, most cases lack clear genetic explanations. Evidence increasingly points to early-life environmental factors as key contributors to ASD, including advanced parental age, maternal diabetes during pregnancy, infections, hormonal imbalances, certain medications, and exposure to air pollution. Currently, ASD diagnosis relies on behavioral assessments, but the absence of specific molecular biomarkers poses significant obstacles to early detection and targeted therapies. Encouragingly, research has identified potential biomarkers, such as neuroimaging classifiers, electroencephalography patterns, eye-tracking data, digital analytics, gene expression profiles, inflammatory and chemokine markers, proteomic and metabolomic profiles, and gut microbiota characteristics. Potential therapeutical strategies under investigation include digital therapies, non-invasive brain stimulation, antioxidants, oxytocin, AVPR1a antagonists, PPAR agonists, and mTOR inhibitors. This review explores ASD across five areas: epidemiological trends, genetic mechanisms, early-life environmental factors and their potential roles, diagnostic biomarkers, and therapeutic approaches.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111411"},"PeriodicalIF":3.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NLRP3 in the dorsal raphe nucleus manipulates the depressive-like behaviors","authors":"Junchao Cai ,&nbsp;Jiarong Zhao ,&nbsp;Rui Peng ,&nbsp;Heming Yu ,&nbsp;Yong He ,&nbsp;Qigang Zhou ,&nbsp;Yue Wang ,&nbsp;Peng Xie","doi":"10.1016/j.brainresbull.2025.111405","DOIUrl":"10.1016/j.brainresbull.2025.111405","url":null,"abstract":"<div><div>Major depressive disorder is one of the most common psychiatric disorders, and the Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome plays an important role in depression. Dorsal raphe nucleus (DRN), as the main origin of producing serotonin in the brain, is an important functional brain region in depressive disorders. However, the relationship between NLRP3 in the DRN and depression has not been clarified in previous studies. So, we focus on demonstrating the role of NLRP3 expressed in DRN in depression. In this study, the male C57BL/6 J mice were exposed to chronic unpredictable mild stimulation and the expression and cellular localization of NLRP3 in DRN were analyzed. Subsequently, the mice were treated with the NLRP3 inhibitor MCC950 to inhibit NLRP3 inflammasome, and the expression of NLRP3 was knocked down in certain cells within the DRN of NLRP3^fl/fl mice to investigate the role of NLRP3 in regulating depressive phenotype. Compared with the control group, the expression of NLRP3 in DRN of CUMS group was significantly increased, especially in the microglia and neuron. Furthermore, treatment with the NLRP3 inhibitor induced a significant antidepressant effect, and the depressive phenotype of NLRP3^fl/fl mice was rescued after knocking down NLRP3 in the microglia or neuron. In addition, the expression levels of related molecules in the NLRP3 inflammasome pathway were significantly higher in the CUMS group compared to the control group. These results illustrated that NLRP3 played an important role in regulating depressive phenotype in DRN, and suggested a new therapy target for depression.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111405"},"PeriodicalIF":3.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144177510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitexin alleviates cerebral ischemia/reperfusion injury by regulating mitophagy via the SIRT1/PINK1/Parkin pathway","authors":"Chao Chen ,&nbsp;Zhenzhong Zhang ,&nbsp;Baolin Du ,&nbsp;Chenling Lv","doi":"10.1016/j.brainresbull.2025.111404","DOIUrl":"10.1016/j.brainresbull.2025.111404","url":null,"abstract":"<div><h3>Objective</h3><div>This study was conducted to elucidate vitexin’s protective effects and underlying mechanism in ameliorating cerebral ischemia/reperfusion injury (CIRI) through regulation of mitophagy.</div></div><div><h3>Methods</h3><div>Focal CIRI in mice was induced using the middle cerebral artery occlusion and reperfusion method. 2,3,5-triphenyltetrazolium chloride staining was performed for the evaluation of cerebral infarction. Neurological deficits and brain tissue damage were assessed by neurological deficit scores and hematoxylin-eosin staining, respectively. HT22 cells underwent oxygen-glucose deprivation/reoxygenation (OGD/R) exposure to develop an <em>in vitro</em> model. Prior to OGD/R, we pretreated the HT22 cells with vitexin, the mitophagy inhibitor (Mdivi-1), or the SIRT1 inhibitor (EX-527). Determination of cell viability and apoptosis were carried out through the cell counting kit-8 assay and flow cytometry, respectively. JC-1 fluorescence staining and MitoSOX™ Red staining were respectively performed for assessing mitochondrial membrane potential (MMP) and detecting levels of mitochondrial reactive oxygen species (mtROS). Expression of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), microtubule-associated protein 1 A/1B-light chain 3 (LC3), sequestosome-1 (p62), PTEN-induced kinase 1 (PINK1), Parkin, as well as silent information regulator two 1 (SIRT1) was determined via Western blot.</div></div><div><h3>Results</h3><div>Vitexin was found to significantly alleviate CIRI in mice and mitigate HT22 cell injury due to OGD/R exposure, as confirmed by our <em>in vivo</em> and <em>in vitro</em> experiments, accompanied by activation of mitophagy and the SIRT1/PINK1/Parkin pathway. The OGD/R+Vitexin+Mdivi-1 group (versus the OGD/R+Vitexin group) displayed decreased cell viability, increased apoptosis, a reduced Bcl-2/Bax ratio, diminished MMP, elevated mtROS levels, downregulated PINK1, LC3-II, and Parkin expression, and upregulated p62 expression. Similarly, the OGD/R+Vitexin+EX-527 group showed reduced cell viability, increased apoptosis, a decreased Bcl-2/Bax ratio, decreased MMP, elevated mtROS levels, downregulated SIRT1, PINK1, LC3-II, and Parkin expression, and upregulated p62 expression.</div></div><div><h3>Conclusion</h3><div>Vitexin ameliorates CIRI by activating mitophagy via the SIRT1/PINK1/Parkin pathway.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111404"},"PeriodicalIF":3.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144167775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-epileptic and gut-protective effects of trioctanoin and the critical role of gut microbiota in a mouse model of epilepsy","authors":"Fei Yu ,&nbsp;Jia-Lin Ji ,&nbsp;Ying Wang ,&nbsp;Yi-Di Liu ,&nbsp;Yi-Mei Lian ,&nbsp;Meng-Zhen Wang ,&nbsp;Zheng-Xu Cai","doi":"10.1016/j.brainresbull.2025.111401","DOIUrl":"10.1016/j.brainresbull.2025.111401","url":null,"abstract":"<div><div>Gut microbiota structure and function affect metabolism, gut health, and behavioral responses and are regulated by dietary factors. Recent research suggests the association of the gut-brain axis with epilepsy pathogenesis, thus offering potential new therapeutic targets. This study evaluated the anti-epileptic effect of trioctanoin and explored the potential role of the gut microbiota in a chronic pentylentetrazol (PTZ)-induced seizure mouse model. Behavioral assessments, electroencephalogram monitoring, immunofluorescence staining, neurotransmitter detection, gut microbiota sequencing, intestinal barrier function tests, and Fecal Microbiota Transplantation (FMT) were performed to systematically study the anti-epileptic effects of trioctanoin and the potential role of microbiota. Trioctanoin significantly restored glial cell proliferation to normal levels in chronic PTZ mice. Moreover, trioctanoin reduced elevated glutamate levels in the hippocampus of PTZ mice and improved gut microbiota imbalance and gut health by restoring the abundance of <em>Dubosiella</em> and <em>Faecalibaculum</em> genera, upregulating tight junction protein expression in the colon, and decreasing elevated levels of the inflammatory markers. Antibiotics(Abx) pre-treatment abolished the anticonvulsant protective effect of Trioctanoin. Although the FMT experiment did not transfer the anticonvulsant protection to the Abx+PTZ group mice, the results suggest that FMT still partially restored the gut microbiota imbalance in the chronic PTZ-induced epilepsy mouse model. These results provide new insights into dietary and gut microbiota-based therapeutic strategies for epilepsy.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111401"},"PeriodicalIF":3.5,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The decrease of GluN2B and its phosphorylation at Tyr-1336 in extrasynaptic subunits is associated with neuroprotection induced by hypoxia preconditioning","authors":"Haidong Hou ,&nbsp;Jing Yang ,&nbsp;Gang Fu ,&nbsp;Xiaolei Liu ,&nbsp;You Liu ,&nbsp;Kerui Gong ,&nbsp;Ruifang Qi ,&nbsp;Xiangning Jiang ,&nbsp;Guo Shao","doi":"10.1016/j.brainresbull.2025.111400","DOIUrl":"10.1016/j.brainresbull.2025.111400","url":null,"abstract":"<div><div>Prior research has firmly established that the N-methyl-d-aspartate (NMDA) receptor subunit 2 B (GluN2B) and its phosphorylation contribute to ischemic/hypoxic brain injury. Hypoxic preconditioning (HPC) is an endogenous mechanism that protects the brain from both ischaemic and hypoxic damage. In this study, we explored the effects of HPC on GluN2B and its phosphorylation at two sites (tyrosine residues 1252 and 1336), catalysed by Fyn, in the hippocampus both <em>in vivo</em> and <em>in vitro.</em> Animal and cellular models of HPC were developed by subjecting mice and the mouse hippocampal neuronal cell line HT22 to repeated hypoxia. Levels of GluN2B and its phosphorylation at the tyrosine residues 1336 (pY1336 GluN2B) and 1252 (pY1252 GluN2B) were detected in HPC-treated hippocampi and HT22 cells using western blotting and immunofluorescence. The distributions of GluN2B, pY1336 GluN2B, and pY1252 GluN2B in the synaptic (TxP) and extrasynaptic components (TxS) were analysed by western blotting. Caspase-3 and spectrin, both markers of cellular injury, were further measured using western blotting. HPC downregulated GluN2B and pY1336 GluN2B levels in the hippocampus and HT22 cells. The changes in GluN2B and pY1336 GluN2B levels in the extrasynaptic components were similar to those in the hippocampus and HT22 cells, while the changes in the synaptic components showed the opposite trend which increased after HPC. The downregulation of GluN2B and pY1336 GluN2B may be associated with neuroprotection induced by HPC. Additionally, their localization at synaptic and extrasynaptic sites may play distinct roles in neuroprotection.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111400"},"PeriodicalIF":3.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expansion of white matter hyperintensities is associated with the glymphatic system dysfunction in cerebral small vessel disease","authors":"Bang Zeng ,&nbsp;Peng Zeng ,&nbsp;Yayun Xiang ,&nbsp;Yuling Peng ,&nbsp;Dan Luo ,&nbsp;Binglan Li ,&nbsp;Ying Chai ,&nbsp;Dan Wang ,&nbsp;Lisha Nie ,&nbsp;Yongmei Li","doi":"10.1016/j.brainresbull.2025.111391","DOIUrl":"10.1016/j.brainresbull.2025.111391","url":null,"abstract":"<div><h3>Objectives</h3><div>To explore the relationship between the glymphatic system and various patterns of white matter hyperintensities (WMHs) in the early stages of cerebral small vessel disease (CSVD), as well as their impact on cognitive function.</div></div><div><h3>Methods</h3><div>The report included 84 patients with CSVD and 23 healthy controls (HCs). To comprehensively assess the impact of white matter hyperintensity volume (WMHV) and WMH counts, we introduced the mean WMHV (WMHV/count) as a new biomarker. Using a threshold of 0.1 for mean WMHV, we categorized participants into two groups to compare intergroup differences. The metrics of the glymphatic system included the index of diffusivity along the perivascular space (Analysis aLong the Perivascular Space [ALPS] index) and the fractional volume of free water (FW). Finally, we analyzed the correlations between imaging indicators and cognitive scales using linear regression models.</div></div><div><h3>Results</h3><div>Compared to HC and Group 1 (mean WMHV ≤ 0.1), Group 2 (mean WMHV &gt; 0.1) exhibited a lower ALPS index and higher fractional volume of FW across various brain regions, including the whole brain (FW-ALL), white matter (FW-WM), basal ganglia (FW-BG), and hippocampus (FW-Hipp). In a correlation analysis, the mean WMHV showed significant correlations with FW-ALL, FW-WM, and FW-BG. Meanwhile, WMHV was only correlated with FW-BG. Furthermore, both FW-BG and the ALPS index were associated with Digit Symbol Substitution Test scores.</div></div><div><h3>Conclusions</h3><div>Mean WMHV can reflect the confluence and expansion of WMH and is closely associated with glymphatic system disfunction.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111391"},"PeriodicalIF":3.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations of white matter functional networks in pediatric drug-resistant temporal lobe epilepsy: A graph theory analysis study","authors":"Kexin Huang ,&nbsp;Yuxin Xie ,&nbsp;Haifeng Ran ,&nbsp;Jie Hu ,&nbsp;Yulun He ,&nbsp;Gaoqiang Xu ,&nbsp;Guiqin Chen ,&nbsp;Qiane Yu ,&nbsp;Xuhong Li ,&nbsp;Junwei Liu ,&nbsp;Heng Liu ,&nbsp;Tijiang Zhang","doi":"10.1016/j.brainresbull.2025.111403","DOIUrl":"10.1016/j.brainresbull.2025.111403","url":null,"abstract":"<div><div>Neurological disorder can cause functional network changes in white matter (WM). However, changes in the WM functional network in children with drug-resistant temporal lobe epilepsy (DRTLE) require further clarification. Therefore, we combine graph theory with resting-state functional magnetic resonance imaging (rs-fMRI) and T₁-weighted imaging (T₁WI) to investigate the topological features of the WM network in children with DRTLE, discover potential biomarkers, and understand the underlying neurological mechanisms. We included 91 children (43 with DRTLE and 48 healthy controls), acquiring structural and functional MRI data to construct WM functional networks. Graph theory was applied to evaluate topological differences and their correlation with onset age, disease duration and cognitive measures. A Support Vector Machine model classified individuals with DRTLE based on WM connectivity, with accuracy validated through leave-one-out cross-validation. The global topological properties of the WM network in children with DRTLE were altered, manifesting as an imbalance between global integration and segregation Local nodal efficiency changes in the association fibers exhibited reduced information transfer and centrality at several nodes. Conversely, commissural and projection fibers displayed increased network properties. Cognitive metrics correlated with nodal disturbances. The classification model achieved 73.6 % accuracy and an area under the curve (AUC) of 0.744. This indicates that the WM functional network in DRTLE presents with anomalies in the topological attributes, which are associated with cognitive impairments. The WM functional connectivity may serve as valuable indicators for clinical classification of the condition. The insights provided have augmented our understanding of the complex neurological mechanisms involved in epilepsy.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111403"},"PeriodicalIF":3.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144139485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the neural dynamics of mathematical interference in english reading: A novel approach with deep learning and fNIRS data","authors":"Zhijie Liang ,&nbsp;Ling Wang ,&nbsp;Jianyu Su ,&nbsp;Bo Sun ,&nbsp;Daifa Wang ,&nbsp;Juan Yang","doi":"10.1016/j.brainresbull.2025.111398","DOIUrl":"10.1016/j.brainresbull.2025.111398","url":null,"abstract":"<div><div>English has emerged as the predominant global language, driving efforts to optimize its acquisition through interdisciplinary cognitive research. While behavioral studies suggest a link between English learning and mathematical cognition, the neural mechanisms underlying this relationship remain poorly understood. To bridge this gap, the present study employs functional near-infrared spectroscopy (fNIRS) to construct a novel dataset on mathematical interference in English acquisition. Utilizing this dataset, a novel deep learning model named AC-LSTM is proposed, amalgamating Transformer and LSTM architectures to identify residual mathematical cognition during the English learning process. The AC-LSTM model achieves an exceptional accuracy rate of 99.8 %, surpassing other machine learning and deep learning models. Moreover, a multi-class classification experiment is conducted to discern algebra, geometry, and quantitative reasoning interference, with the AC-LSTM model achieving the highest accuracy of 75.9 % in this classification task. Furthermore, crucial brain channels for interference detection are pinpointed through grid search, and alterations in vital brain regions (R-Broca and L-Broca) are unveiled via association rule analysis. By integrating fNIRS, deep learning, and data mining techniques, this study delves into cognitive interference in English learning, providing valuable insights for educational neuroscience and data mining research.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111398"},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative metabolomics and transcriptomics analysis of hippocampus reveals taurine metabolism and sphingolipid metabolism dysregulation associated with sleep deprivation-induced memory impairment","authors":"Ting Chen ,&nbsp;Junke Jia ,&nbsp;Chenyi Gao ,&nbsp;Qi Zhong ,&nbsp;Lijuan Tang ,&nbsp;Xiaokai Sui ,&nbsp;Shuang Li ,&nbsp;Chang Chen ,&nbsp;Zongze Zhang","doi":"10.1016/j.brainresbull.2025.111397","DOIUrl":"10.1016/j.brainresbull.2025.111397","url":null,"abstract":"<div><div>Sleep plays a crucial role in restoring and repairing the body, consolidating memory, regulating emotions, maintaining metabolic and so on. Sleep deprivation is known to impair cognitive functions. In this study, we investigated the mechanisms underlying memory impairment induced by sleep deprivation through a combined metabolomic and transcriptomic analysis of hippocampus. Eight-week-old mice were selected as the study subjects and the sleep deprivation chamber was used to establish a sleep deprivation model. Novel object recognition tests (NOR), and Y-maze tests were used to assess the behavioral outcomes in mice. The hippocampus were extracted and studied using the untargeted metabolomics or transcriptomics high-throughput sequencing method. An integrative analysis was conducted to elucidate the metabolic and genetic changes. Behavioral tests showed that sleep-deprived mice exhibited memory impairment. Metabolomic analysis identified 84 differentially expressed metabolites (DEMs), including 12 under the positive ion mode and 72 under the negative ion mode. The analysis revealed that sleep deprivation caused abnormalities in several metabolic pathways, with particularly pronounced effects observed in glycerophospholipid metabolism, linoieic acid metabolism, alanine, aspartate, glutamate metabolism, taurine and hypotaurine metabolism, and purine metabolism. While transcriptomic analysis releaved 97 differentially expressed genes (DEGs) (51 were down-regulated and 46 were up-regulated DEGs). Integrative analysis of the metabolomic and transcriptomic identified profiles showed that sleep deprivation may regulate taurine and hypotaurine metabolism and sphingolipid metabolism, there by influencing memory. Our results prompt severe metabolic disturbances occur in the hippocampus with sleep deprivation in mice, which can provide a basis for the mechanism research.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111397"},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of changes in the interaction of cerebral cortex during the oral swallowing task","authors":"Yusi Zhang ,&nbsp;Xiuyu Li ,&nbsp;Jiaqiu Lin ,&nbsp;Xiaoyin Mao ,&nbsp;Yating Wu ,&nbsp;Huimin Hu ,&nbsp;Jiaxin Lin ,&nbsp;Yan Wang ,&nbsp;Huajun Yang ,&nbsp;Dongmei Fu ,&nbsp;Qingqing Zhang ,&nbsp;Yan Zhan","doi":"10.1016/j.brainresbull.2025.111399","DOIUrl":"10.1016/j.brainresbull.2025.111399","url":null,"abstract":"<div><h3>Background</h3><div>The main swallowing activities in the oral phase include chewing and tongue movements. Cortical control is essential for the initiation and coordination of swallowing activities in the oral phase.</div></div><div><h3>Research purposes</h3><div>This study aims to further investigate whether there are differences neural mechanisms in cortical interactions underlying oral phase by simulating chewing and tongue movement.</div></div><div><h3>Methods</h3><div>This study recruited 25 healthy adult participants, by functional magnetic resonance imaging to collect data in the Empty chewing task and Tongue-to-Palate posterior Retraction task. The Dynamic causal modelling and Parametric Empirical Bayes were used to analyze the best model and the effective connectivity between brain regions under different tasks.</div></div><div><h3>Results</h3><div>In the Empty Chewing task, the primary motor cortex(M1) is the main driving input brain area with significant excitatory connectivity with the primary somatosensory cortex(S1) and supplementary motor area(SMA). However, in the Tongue-to-Palate posterior Retraction task, S1 becomes the main driving input brain area and maintains bidirectional connections with M1 and SMA, but S1 shows an inhibitory effect on SMA.</div></div><div><h3>Conclusion</h3><div>This study reveals the differences in the interaction among brain regions during the oral swallowing activity. Results suggest M1 and SMA interaction is vital for the whole oral phase. M1 is a key brain region for Empty chewing task, while S1 is important for sensory feedback. S1 may inhibit SMA during the Tongue-to-Palate posterior Retraction task to aid swallowing and reduce interference with the pharyngeal swallowing action.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"227 ","pages":"Article 111399"},"PeriodicalIF":3.5,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144132133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}