Frontiers in Cellular Neuroscience最新文献

{"title":"Corrigendum: Hypidone hydrochloride (YL-0919) produces a fast-onset reversal of the behavioral and synaptic deficits caused by chronic stress exposure.","authors":"Yuhua Ran, Zengliang Jin, Xiaofei Chen, Nan Zhao, Xinxin Fang, Liming Zhang, Youzhi Zhang, Yunfeng Li","doi":"10.3389/fncel.2025.1558690","DOIUrl":"https://doi.org/10.3389/fncel.2025.1558690","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2018.00395.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1558690"},"PeriodicalIF":4.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress of DNA methylation on the regulation of substance use disorders and the mechanisms.","authors":"Ya Liu, Xiao-Qian Wang, Peng Zhang, Abbas Haghparast, Wen-Bin He, Jian-Jun Zhang","doi":"10.3389/fncel.2025.1566001","DOIUrl":"https://doi.org/10.3389/fncel.2025.1566001","url":null,"abstract":"<p><p>Drug abuse can damage the central nervous system and lead to substance use disorder (SUD). SUD is influenced by both genetic and environmental factors. Genes determine an individual's susceptibility to drug, while the dysregulation of epigenome drives the abnormal transcription processes, promoting the development of SUD. One of the most widely studied epigenetic mechanisms is DNA methylation, which can be inherited stably. In ontogeny, DNA methylation pattern is dynamic. DNA dysmethylation is prevalent in drug-related psychiatric disorders, resulting in local hypermethylation and transcriptional silencing of related genes. In this review, we summarize the role and regulatory mechanisms of DNA methylation in cocaine, opioids, and methamphetamine in terms of drug exposure, addiction memory, withdrawal relapse, intergenerational inheritance, and focus on cell-specific aspects of the studies with a view to suggesting possible therapeutic regimens for targeting methylation in both human and animal research.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1566001"},"PeriodicalIF":4.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A vascular endothelial cell, neuron, and microglia tri-culture model to study hypertension-related depression.","authors":"Hongxia Zhao, Lingge Huang, Jian Liu, Min Feng, Yeqian Liu, Hong Li, Shan Gong, Chunming Chen, Shuiqing Zeng, Weiqiong Ren","doi":"10.3389/fncel.2025.1553309","DOIUrl":"https://doi.org/10.3389/fncel.2025.1553309","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Hypertension-related Depression (HD) is a complex mental disorder that exerts a significant negative impact on patients' quality of life. Previous studies have demonstrated that damages to vascular endothelial and hippocampus are the primary pathological features in HD rats. Under hypertensive conditions, inflammatory cytokines in peripheral blood vessels can induce central nervous system inflammation through penetration of a damaged blood-brain barrier, peripheral immune cells, and neural pathways, damaging the brain and triggering HD. Therefore, interactions between vascular endothelial cells, neurons, and glial cells are critical for the understanding of HD. However, &lt;i&gt;in vivo&lt;/i&gt; animal models are often limited by the complexity of intrinsic systems, high inter-individual variability, and stringent ethical regulations. A reliable model that could be easily manipulated is needed for investigating the mechanisms involved in communication between vascular endothelial cells, neurons, and glial cells in HD. We therefore aimed to create a composite tri-culture model consisting of rat aortic endothelial cells (RAECs), neurons, and microglia to study HD. First, RAECs were stimulated with lipopolysaccharide to mimic endothelial injury under hypertensive conditions. Vascular endothelial function and inflammatory levels were assessed using fluorescent probes and enzyme-linked immunosorbent assays. RAECs treated with 1 μg/ml LPS for 24 h had reduced levels of nitric oxide, increased levels of endothelin-1 and inflammatory mediators. These findings are consistent with the endothelial dysfunction and inflammatory responses observed in spontaneously hypertensive rats, which suggests that the lipopolysaccharide-induced RAECs model effectively mimics key pathological features of hypertension-related endothelial injury. Subsequently, the supernatants from lipopolysaccharide-induced RAECs were combined with 200 μM corticosterone and transferred to neuron-microglia co-cultures to simulate damages to hippocampal neuron under HD conditions. To evaluate the features of cells, neuronal viability was measured by CCK-8 and live-dead assays. Nissl staining was used to assess neuronal Nissl bodies, while the levels of inflammatory factors and monoamine neurotransmitters in the culture supernatants were evaluated by enzyme-linked immunosorbent assays. Reactive oxygen species in neurons were visualized by a fluorescent probe, apoptosis was detected using TUNEL assays, and immunofluorescence was used to assess microglial phenotypes and the levels of TLR4 and NF-κB. It was found that neurons in the tri-culture model had reduced viability, higher levels of apoptosis, fewer Nissl bodies, increased inflammation, and reduced levels of monoamine neurotransmitters. Additionally, the number of M1 microglia was increased, along with elevated levels of TLR4 and NF-κB proteins. These findings were similar to damages of hippocampal neuron, abnormal levels of monoamine neurotran","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1553309"},"PeriodicalIF":4.2,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11994666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ca²⁺ waves in astrocytes: computational modeling and experimental data.","authors":"Rosa Musotto, Ulderico Wanderlingh, Giovanni Pioggia","doi":"10.3389/fncel.2025.1536096","DOIUrl":"https://doi.org/10.3389/fncel.2025.1536096","url":null,"abstract":"<p><p>This paper examines different computational models for Calcium wave propagation in astrocytes. Through a comparative analysis of models by Goldbeter, De Young-Keizer, Atri, Li-Rinzel, and De Pittà and of experimental data, the study highlights the model contributions for the understanding of Calcium dynamics. Tracing the evolution from simple to complex models, this work emphasizes the importance of integrating experimental data in order to further refine these models. The results allow to improve our understanding of the physiological functions of astrocytes, suggesting the importance of more accurate astrocyte models.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1536096"},"PeriodicalIF":4.2,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11985530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell-type specific epigenetic and transcriptional mechanisms in substance use disorder.","authors":"Bin Wang, Jiale Wang, Nicholas J Beacher, Da-Ting Lin, Yan Zhang","doi":"10.3389/fncel.2025.1552032","DOIUrl":"https://doi.org/10.3389/fncel.2025.1552032","url":null,"abstract":"<p><p>Substance use disorder (SUD) is a chronic and relapse-prone neuropsychiatric disease characterized by impaired brain circuitry within multiple cell types and neural circuits. Recent advancements in single-cell transcriptomics, epigenetics, and neural circuit research have unveiled molecular and cellular alterations associated with SUD. These studies have provided valuable insights into the transcriptional and epigenetic regulation of neuronal and non-neuronal cells, particularly in the context of drug exposure. Critical factors influencing the susceptibility of individuals to SUD include the regulation of gene expression during early developmental stages, neuroadaptive responses to psychoactive substances, and gene-environment interactions. Here we briefly review some of these mechanisms underlying SUD, with an emphasis on their crucial roles in in neural plasticity and maintenance of addiction and relapse in neuronal and non-neuronal cell-types. We foresee the possibility of integrating multi-omics technologies to devise targeted and personalized therapeutic strategies aimed at both the prevention and treatment of SUD. By utilizing these advanced methodologies, we can gain a deeper understanding of the fundamental biology of SUD, paving the way for more effective interventions.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1552032"},"PeriodicalIF":4.2,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11985801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oligodendrocyte arrangement, identification and morphology in the developing superior olivary complex.","authors":"Alina Carola Zacher, Melissa Grabinski, Laura Console-Meyer, Felix Felmy, Christina Pätz-Warncke","doi":"10.3389/fncel.2025.1561312","DOIUrl":"https://doi.org/10.3389/fncel.2025.1561312","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1561312"},"PeriodicalIF":4.2,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11985757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropeptide Y neurons in the basolateral amygdala project to the nucleus accumbens and stimulate high-fat intake.","authors":"Shunji Yamada, Kazunori Kojima, Masaki Tanaka","doi":"10.3389/fncel.2025.1565939","DOIUrl":"https://doi.org/10.3389/fncel.2025.1565939","url":null,"abstract":"<p><p>Neuropeptide Y (NPY) is a 36-amino acid neuropeptide that is widely expressed in the central nervous system, including in the nucleus accumbens (NAc), hypothalamus, and amygdala. The NAc involved in several behaviors, including reward, motivation processes, and feeding behavior. Here, we demonstrate in male mice that NPY input from the basolateral amygdala (BLA) to the NAc is involved in the preferential consumption of a high-fat diet (HFD). First, we demonstrated the NPY input to the NAc from the BLA by injecting adeno-associated virus (AAV)(retro)-FLEX-mCherry into the NAc of NPY-Cre mice. We also confirmed that BLA NPY neurons project exclusively to the NAc by injecting AAV(dj)-hSyn-FLEx -mGFP-2A-Synaptophysin-mRuby into the BLA. Usually, a HFD drives enhanced food intake than a standard chow diet after repetitive exposure. The optogenetic inactivation of BLA NPY neurons projecting to the NAc caused a significant decrease in HFD intake for a 1-h period, while optogenetic activation of these neurons induced the opposite effect. Furthermore, bilateral injection of an NPY receptor type 1 (Y1R) antagonist into the NAc significantly decreased HFD intake for 1-h period compared with vehicle injection, while, conversely, injection of a Y1R agonist enhanced HFD intake. These results suggest that BLA NPY neurons projecting to the NAc mediate preferential HFD intake via NAc-localized Y1R.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1565939"},"PeriodicalIF":4.2,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11983651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Studying the mechanisms of neurodegeneration: <i>C. elegans</i> advantages and opportunities.","authors":"Angie K Torres, Rodrigo G Mira, Cristina Pinto, Nibaldo C Inestrosa","doi":"10.3389/fncel.2025.1559151","DOIUrl":"https://doi.org/10.3389/fncel.2025.1559151","url":null,"abstract":"<p><p><i>Caenorhabditis elegans</i> has been widely used as a model organism in neurodevelopment for several decades due to its simplicity, rapid growth, short life cycle, transparency, and rather simple genetics. It has been useful in modeling neurodegenerative diseases by the heterologous expression of the major proteins that form neurodegenerative-linked aggregates such as amyloid-<i>β</i> peptide, tau protein, and <i>α</i>-synuclein, among others. Furthermore, chemical treatments as well as the existence of several interference RNA libraries, transgenic worm lines, and the possibility of generating new transgenic strains create a magnificent range of possible tools to study the signaling pathways that could confer protection against protein aggregates or, on the contrary, are playing a detrimental role. In this review, we summarize the different <i>C. elegans</i> models of neurodegenerative diseases with a focus on Alzheimer's and Parkinson's diseases and how genetic tools could be used to dissect the signaling pathways involved in their pathogenesis mentioning several examples. Finally, we discuss the use of pharmacological agents in <i>C. elegans</i> models that could help to study these disease-associated signaling pathways and the powerful combinations of experimental designs with genetic tools. This review highlights the advantages of <i>C. elegans</i> as a valuable intermediary between <i>in vitro</i> and mammalian <i>in vivo</i> models in the development of potential new therapies.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1559151"},"PeriodicalIF":4.2,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11979225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Striatal function scrutinized through the PAN-TAN-FSI triumvirate.","authors":"Paul Apicella, Anne-Caroline Martel, Kevin Marche","doi":"10.3389/fncel.2025.1572657","DOIUrl":"10.3389/fncel.2025.1572657","url":null,"abstract":"<p><p>Understanding the information encoded by distinct components of the neuronal circuitry in the striatum represents an avenue for elucidating the role of this subcortical region in adaptive behavior and its dysfunction in pathological conditions. In behaving animals, conventional single neuron recordings generally differentiated between three main electrophysiologically identified neuron subtypes in the striatum, referred to as phasically active neurons (PANs), tonically active neurons (TANs), and fast-spiking interneurons (FSIs), assumed to correspond to GABAergic spiny projection neurons, cholinergic interneurons, and parvalbumin-containing GABAergic interneurons, respectively. Considerable research has been devoted to exploring the behavior-related activities of neurons classified electrophysiologically into PANs, TANs, and FSIs in animals engaged in task performance, mostly monkeys. Although precise neuron identification remains a major challenge, such electrophysiological studies have provided insights into the functional properties of presumed distinct striatal neuronal populations. In this review, we will focus on current ideas about the functions subserved by these neuron subtypes, emphasizing their link to specific aspects of behaviors. We will also underline the issues that are yet to be resolved regarding the classification of striatal neurons into distinct subgroups which emphasize the importance of considering the potential overlap among electrophysiological characteristics and the molecular diversity of neuron types in the striatum.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1572657"},"PeriodicalIF":4.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11975669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum: Epothilone B facilitates peripheral nerve regeneration by promoting autophagy and migration in Schwann cells.","authors":"Jianhua Zhou, Shengyou Li, Jianbo Gao, Yawei Hu, Shaochu Chen, Xinle Luo, Hao Zhang, Zhuojing Luo, Jinghui Huang","doi":"10.3389/fncel.2025.1574709","DOIUrl":"https://doi.org/10.3389/fncel.2025.1574709","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2020.00143.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1574709"},"PeriodicalIF":4.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11975656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}