Experimental Neurobiology最新文献

The Role of Agmatine in Modulating Autophagy Under Neuroinflammatory Conditions Induced by Metabolic Alteration in Mouse Brain. 胍丁氨酸在小鼠脑代谢改变诱导的神经炎症条件下调节自噬的作用。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25007

Ji Young Chang, Jiwon Kim, Jong Youl Kim, Jong Eun Lee

{"title":"The Role of Agmatine in Modulating Autophagy Under Neuroinflammatory Conditions Induced by Metabolic Alteration in Mouse Brain.","authors":"Ji Young Chang, Jiwon Kim, Jong Youl Kim, Jong Eun Lee","doi":"10.5607/en25007","DOIUrl":"10.5607/en25007","url":null,"abstract":"Changes in microglia, a specialized population of glial cells found in the central nervous system (CNS), is often associated with hyperglycemic conditions. It has been reported that exogenous administration of agmatine (agm) has neuroprotective effects in CNS injuries, including neurodegenerative diseases, while also being involved with modulating macrophage subdivision. In this study, the effects of agmatine on microglial polarization has been investigated and whether this effect can be related to the modulation of autophagy in neuroinflammatory conditions induced by high glucose (HG) concentrations. Neuroinflammatory conditions were mimicked through treatment to BV2 microglial cells. BV2 cells were mainly induced into proinflammatory M1 phenotype when treated with HG (100 mM), shown by the increase in M1 marker, CD86, and shifted to M2 phenotype in HG condition with agm (100 μM), indicated by the upregulation of mannose receptor CD206. When agm was treated with HG, the level of LC3-II was increased while p62/SQSTM1 level was downregulated, and the expression of LAMP1 was increased. In transmission electron microscopy, autophagosomes has shown that HG conditions led to severe mitochondrial damage while elongating phagophore membranes and autolysosomes were seen in cells treated with HG and agm, showing stimulated mitophagy. In a high-fat diet-induced T2DM metabolic dementia animal model, agmatine administration upregulated autophagy and shifted microglial polarization from proinflammatory to anti-inflammatory phenotype, improving cognitive function and alleviating neuroinflammation. In this study, it has been demonstrated that agm treatment can ameliorate neuroinflammation by upregulating autophagy on a cellular level and shifting microglia polarization from M1 to M2 phenotype, showing a therapeutic potential in metabolic AD.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"95-107"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552794","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}

引用次数: 0

Domain-generalized Deep Learning for Improved Subject-independent Emotion Recognition Based on Electroencephalography. 基于脑电图的改进主题无关情绪识别的领域广义深度学习。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 Epub Date: 2025-05-14 DOI: 10.5607/en25011

Jung-Hwan Kim, Hyerin Nam, Doyeon Won, Chang-Hwan Im

{"title":"Domain-generalized Deep Learning for Improved Subject-independent Emotion Recognition Based on Electroencephalography.","authors":"Jung-Hwan Kim, Hyerin Nam, Doyeon Won, Chang-Hwan Im","doi":"10.5607/en25011","DOIUrl":"10.5607/en25011","url":null,"abstract":"Electroencephalography (EEG) provides high temporal resolution and noninvasiveness for a range of practical applications, including emotion recognition. However, inherent variability across subjects poses significant challenges to model generalizability. In this study, we systematically evaluated twelve approaches by combining four domain generalization (DG) techniques, Deep CORAL, GroupDRO, VREx, and DANN, with three representative deep learning architectures (ShallowFBCSPNet, EEGNet, and TSception) to enable improved subject-independent EEG-based emotion recognition. The performances of the DG-integrated deep learning models were quantitatively evaluated using two emotional EEG datasets collected by the authors. Data from each subject were treated as distinct domains in each model. Binary classification tasks were conducted to identify the valence or arousal state of each participant based on a ten-fold cross-validation strategy. The results indicated that the application of DG methods consistently enhanced classification accuracy across datasets. In one dataset, TSception combined with VREx achieved the highest performance for both valence and arousal classifications. In the other dataset, TSception with VREx still yielded the highest valence classification accuracy, while TSception combined with GroupDRO showed the best arousal classification performance among the twelve models, slightly outperforming TSception with VREx. These findings underscore the potential of DG approaches to mitigate distributional shifts caused by intersubject and intersession variabilities to implement robust subject-independent EEG-based emotion recognition systems.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":"119-130"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971614","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}

引用次数: 0

The Neurotoxic Properties of α-synuclein Polymorphs. α-突触核蛋白多态性的神经毒性。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25016

Katherine Chang, Zulfeqhar Syed, Valentina Baena, Mark R Cookson, Changyoun Kim

{"title":"The Neurotoxic Properties of α-synuclein Polymorphs.","authors":"Katherine Chang, Zulfeqhar Syed, Valentina Baena, Mark R Cookson, Changyoun Kim","doi":"10.5607/en25016","DOIUrl":"10.5607/en25016","url":null,"abstract":"Progressive neurodegeneration is a common pathological feature of synucleinopathies, which include dementia with Lewy bodies (DLB), Parkinson's disease (PD), and multiple system atrophy (MSA). Among mechanisms known to induce neurodegeneration, the presence of aggregated forms of α-synuclein (α-syn) has been extensively considered as a causal factor for cell death. These aggregates exist in multiple different physical forms, which might yield different disease phenotypes and explain the heterogeneity among these diseases. Here, we investigated the neurotoxic properties of structurally distinct and exogenous α-syn polymorphs. Most of the polymorphs at the concentrations we studied are neurotoxic, but dopamine stabilized α-syn oligomer induced greater levels of neurotoxicity at lower concentrations compared to other polymorphs. In addition, polymorphs commonly induced apoptotic neuronal death through autophagic impairment. Our results suggest that neurons have different sensitivities to different α-syn aggregates, which should be a consideration when developing disease markers and therapeutics.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"87-94"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552793","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}

引用次数: 0

Robust Neuroprotection by NEMO (IKKγ)-binding Domain Peptide via Anti-inflammatory Effects in the Post-ischemic Brain. NEMO （IKKγ）结合区域肽通过抗炎作用在缺血后脑中的强大神经保护作用

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-06-30 DOI: 10.5607/en25020

Sang-A Oh, Song-I Seol, Ja-Kyeong Lee, Il-Doo Kim

{"title":"Robust Neuroprotection by NEMO (IKKγ)-binding Domain Peptide via Anti-inflammatory Effects in the Post-ischemic Brain.","authors":"Sang-A Oh, Song-I Seol, Ja-Kyeong Lee, Il-Doo Kim","doi":"10.5607/en25020","DOIUrl":"10.5607/en25020","url":null,"abstract":"Microglia exhibit a complex and context-dependent role in the post-ischemic brain, performing both neuroprotective and neurotoxic functions. Among the many factors contributing to pro-inflammatory microglia activation, NF-κB signaling plays a pivotal role. The NEMO (IKKγ)-binding domain (NBD) peptide, an 11-amino-acids cell-permeable peptide spanning the NBD of IKKα and IKKβ, acts as a highly specific inhibitor by preventing NEMO-IKKα/IKKβ complex formation. We investigated the neuroprotective effects of the NBD peptide in a post-ischemic brain using a transient middle cerebral artery occlusion (MCAO) animal model. In in vitro experiments, pre-treatment of BV2 cells (a microglia cell line) with NBD peptide significantly suppressed LPS-induced NEMO-IKKα/IKKβ complex formation, nuclear translocation of p65, and upregulation of numerous pro-inflammatory cytokines expressions. The anti-inflammatory effect was further confirmed in reporter gene assay following reporter plasmid transfection, demonstrating a NBD peptide dose-dependent response. In the post-ischemic brain, intranasal delivery of NBD peptide significantly suppressed NEMO-IKKα/IKKβ complex formation, IκB-α phosphorylation, microglial activation, and cytokine induction. Notably, intranasal administration of NBD peptide 3 h post-MCAO significantly reduced infarct volumes in a dose-dependent manner. A significant reduction in infarct volume was observed by 6 h post-administration, suggesting an extended therapeutic window for the NBD peptide. These neuroprotective effects were accompanied by the attenuation of neurological deficits and motor function impairment, as assessed by rota-rod, beam balance, and corner turn tests. Collectively, these results highlight a robust neuroprotective effect along with long-term outcomes of NBD peptide in the post-ischemic brain, with NBD peptide-mediated blocking of NEMO-IKKα/IKKβ complex formation serving as a key underlying molecular mechanism.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 3","pages":"108-118"},"PeriodicalIF":1.8,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552792","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}

引用次数: 0

Celiac Disease Increases the Risk of Multiple Sclerosis: Evidence from Mendelian Randomization and the Role of CCL19. 乳糜泻增加多发性硬化症的风险：来自孟德尔随机化和CCL19作用的证据

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-04-30 Epub Date: 2025-04-15 DOI: 10.5607/en25009

Seongjin Lim, Junhua Wu, Yeon Woo Kim, Sun Woo Lim, Juhee Shin, Hyo Jung Shin, Sang Ryong Kim, Dong Woon Kim

{"title":"Celiac Disease Increases the Risk of Multiple Sclerosis: Evidence from Mendelian Randomization and the Role of CCL19.","authors":"Seongjin Lim, Junhua Wu, Yeon Woo Kim, Sun Woo Lim, Juhee Shin, Hyo Jung Shin, Sang Ryong Kim, Dong Woon Kim","doi":"10.5607/en25009","DOIUrl":"10.5607/en25009","url":null,"abstract":"Celiac disease (CeD) is an autoimmune disorder triggered by gluten, primarily affecting the small intestine but potentially impacting other systems, including the nervous system through the gut-brain axis. This study employed Mendelian randomization (MR) to explore the causal relationships between CeD and several neurological disorders, with a particular focus on multiple sclerosis (MS). Utilizing genetic data from the OpenGWAS and Finngen databases, we applied various MR methods, including Inverse Variance Weighted (IVW), IVW-multiplicative random effects (MRE), weighted median (WM), MR-Egger, and robust adjusted profile score (RAPS), to investigate these associations. The analysis revealed no significant causal relationship between CeD and several other neurological disorders, but a significant positive association with MS was found (IVW OR=1.1919, 95% CI: 1.0851~1.3092, p=0.0002). Further analysis indicated that the mediator CCL19 plays a significant role in the pathway from CeD to MS, suggesting that CCL19 may be a key factor in the immune response linking these conditions. This mediation effect highlights the potential mechanism through which CeD increases the risk of developing MS. These findings emphasize the complexity of the relationship between CeD and MS, indicating the need for further research to understand these connections better and their clinical implications.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"63-76"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062690","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}

引用次数: 0

Magnesium-L-threonate Ameliorates Cognitive Deficit by Attenuating Adult Hippocampal Neurogenesis Impairment in a Mouse Model of Alzheimer's Disease. 镁- l -苏酸钠通过减轻阿尔茨海默病小鼠模型的成年海马神经发生损伤来改善认知缺陷

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-04-30 Epub Date: 2025-04-16 DOI: 10.5607/en24030

Ying Xiong, Yuwen Yang, Yuting Ruan, Wencai Ou, Zhiwen Hu, Wei Li, Nina Xiao, Wang Liao, Jianhua Liu, Zhenlu Liu, Qiong Luo, Feifei Liu, Jun Liu

{"title":"Magnesium-L-threonate Ameliorates Cognitive Deficit by Attenuating Adult Hippocampal Neurogenesis Impairment in a Mouse Model of Alzheimer's Disease.","authors":"Ying Xiong, Yuwen Yang, Yuting Ruan, Wencai Ou, Zhiwen Hu, Wei Li, Nina Xiao, Wang Liao, Jianhua Liu, Zhenlu Liu, Qiong Luo, Feifei Liu, Jun Liu","doi":"10.5607/en24030","DOIUrl":"10.5607/en24030","url":null,"abstract":"Impaired adult hippocampal neurogenesis is a key pathological mechanism contributing to memory deficits in Alzheimer's disease (AD). Recent studies have shown that elevating magnesium levels promotes neurogenesis by enhancing the neuronal differentiation of adult neural progenitor cells in vitro. Therefore, this in vivo study aims to determine if magnesium-L-threonate (MgT) can ameliorate cognitive deficit of AD mice by attenuating adult hippocampal neurogenesis impairment and to reveal the underlying mechanisms. APPswe/PS1dE9 mice were treated with different doses of MgT and ERK inhibitor PD0325901. The memory ability of each mouse was recorded by Morris Water Maze test. After cognitive test, hippocampus tissues were collected to measure the proportion of BrdU/doublecortin double-labeled cells using the flow cytometry test and assess the expression of doublecortin using PCR and Western blot. Furthermore, the activations of CREB, ERK, P38 and JNK were measured by Western blot to identify the involved mechanisms. The cognitive test confirmed that MgT treatment attenuated the memory impairment of APPswe/PS1dE9 mice. Flow cytometry test showed that Brdu/doublecortin labeled newborn neurons gradually increased following MgT administration. In line with the flow cytometry results, Western blot and PCR confirmed that MgT administration significantly increased doublecortin expression levels. Furthermore, the ratios of p-ERK/ERK and p-CREB/CREB increased with MgT elevation. In addition, these effects of MgT treatment were markedly reversed by PD0325901 supplementation. In conclusion, MgT treatment improved cognitive decline by ameliorating adult hippocampal neurogenesis impairment in this AD model, possibly via ERK/CREB activation.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"53-62"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989861","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}

引用次数: 0

Astrocytic Ornithine Decarboxylase 1 in Alzheimer's Disease. 阿尔茨海默病星形细胞鸟氨酸脱羧酶1。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-04-30 Epub Date: 2025-04-11 DOI: 10.5607/en25006

Mridula Bhalla, C Justin Lee

引用次数: 0

Modeling Temporal Dependencies in Brain Functional Connectivity to Identify Autism Spectrum Disorders Based on Heterogeneous rs-fMRI Data. 基于异质rs-fMRI数据的脑功能连接时间依赖性建模以识别自闭症谱系障碍。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-04-30 DOI: 10.5607/en24028

Yaya Liu, Qiang Zhao, Lishuang Zhao, Yanchun Liu, Xiaoli Li

{"title":"Modeling Temporal Dependencies in Brain Functional Connectivity to Identify Autism Spectrum Disorders Based on Heterogeneous rs-fMRI Data.","authors":"Yaya Liu, Qiang Zhao, Lishuang Zhao, Yanchun Liu, Xiaoli Li","doi":"10.5607/en24028","DOIUrl":"10.5607/en24028","url":null,"abstract":"Brain functional connectivity has shown promise for developing objective biomarkers for autism spectrum disorder (ASD). Although many imaging studies have demonstrated its potential, most have focused on static measurements. In this study, we explored the dynamic changes in functional connectivity over time to uncover potential temporal dependencies. These dynamic patterns were abstracted into high-level representations and used as predictors to identify individuals at risk of ASD. To achieve this, we employed a deep learning framework that combines attention mechanism with long short-term memory (LSTM) neural network. Experiments were conducted using heterogeneous resting-state functional magnetic resonance imaging (rs-fMRI) data from the Autism Brain Imaging Data Exchange (ABIDE) database. The resulting classification achieved an accuracy of 74.9% and precision of 75.5% under intra-site cross-validation, outperforming traditional classifiers such as support vector machines (SVM), random forests (RF), and single LSTM network. Further analyses demonstrated the robustness and generalizability of our model, with classification performance less affected by subjects' gender or age. The optimal model's weights revealed atypical temporal dependencies in the brain functional connectivity of individuals with ASD, highlighting the potential for these patterns to serve as biomarkers. Our findings underscore the importance of dynamic functional connectivity in understanding ASD and suggest that our deep learning framework could aid in the development of more accurate and reliable diagnostic tools for this disorder.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"77-86"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990508","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}

引用次数: 0

Neuroinflammation in Adaptive Immunodeficient Mice with Colitis-like Symptoms. 具有结肠炎样症状的适应性免疫缺陷小鼠的神经炎症

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-02-28 DOI: 10.5607/en24016

Sung Hee Park, Junghwa Kang, Ji-Young Lee, Jeong Seon Yoon, Sung Hwan Hwang, Ji Young Lee, Deepak Prasad Gupta, Il Hyun Baek, Ki Jun Han, Gyun Jee Song

{"title":"Neuroinflammation in Adaptive Immunodeficient Mice with Colitis-like Symptoms.","authors":"Sung Hee Park, Junghwa Kang, Ji-Young Lee, Jeong Seon Yoon, Sung Hwan Hwang, Ji Young Lee, Deepak Prasad Gupta, Il Hyun Baek, Ki Jun Han, Gyun Jee Song","doi":"10.5607/en24016","DOIUrl":"10.5607/en24016","url":null,"abstract":"Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis. Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"34-47"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647857","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}

引用次数: 0

Transcriptomic Alteration in the Brain and Gut of Offspring Following Prenatal Exposure to Corticosterone. 产前暴露于皮质酮后后代大脑和肠道的转录组改变。

IF 1.8 4区医学

Experimental Neurobiology Pub Date : 2025-02-28 DOI: 10.5607/en24029

Eun-A Ko, Tong Zhou, Jae-Hong Ko, Sung-Cherl Jung

{"title":"Transcriptomic Alteration in the Brain and Gut of Offspring Following Prenatal Exposure to Corticosterone.","authors":"Eun-A Ko, Tong Zhou, Jae-Hong Ko, Sung-Cherl Jung","doi":"10.5607/en24029","DOIUrl":"10.5607/en24029","url":null,"abstract":"Maternal stress during pregnancy can profoundly affect offspring health, increasing the risk of psychiatric disorders, metabolic diseases, and gastrointestinal problems. In this study, the effects of high prenatal corticosterone exposure on gene expression in the brain and small intestine of rat offspring were investigated via RNA-sequencing analysis. Pregnant rats were divided into two groups: Corti.Moms were injected with corticosterone daily, while Nor.Moms were given saline injections. Their offspring were labeled as Corti.Pups and Nor.Pups, respectively. The brain tissue analysis of Corti.Pups showed that the expression levels of the genes linked to neurodegenerative conditions increased and enhanced mitochondrial biogenesis, possibly due to higher ATP demands. The genes associated with calcium signaling pathways, neuroactive ligand-receptor interactions, and IgA production were also upregulated in the small intestine of Corti.pups. Conversely, the genes related to protein digestion, absorption, and serotonergic and dopaminergic synaptic activities were downregulated. These findings revealed that gene expression patterns in both the brain and intestinal smooth muscle of offspring prenatally exposed to corticosterone were substantially altered. Thus, this study provided valuable insights into the effects of prenatal stress on neurodevelopment and gut function.","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"9-19"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647858","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}

引用次数: 0