Frontiers in Cellular Neuroscience最新文献

{"title":"Diversity of glutamate receptors in glial cells of the mouse optic nerve.","authors":"Nine F Kompier, Marcus Semtner, Sophie Walter, Christian Steinhäuser, Christiane Nolte, Helmut Kettenmann","doi":"10.3389/fncel.2026.1911068","DOIUrl":"10.3389/fncel.2026.1911068","url":null,"abstract":"<p><strong>Introduction: </strong>Glial cells in the optic nerve express ionotropic glutamate receptors that may contribute to axon-glia communication, yet their functional expression in defined glial populations remains incompletely characterized. We investigated glutamate receptor-mediated responses in identified NG2 glia and astrocytes of the mouse optic nerve.</p><p><strong>Methods: </strong>We used a longitudinal optic nerve slice preparation combined with whole-cell patch-clamp recordings. NG2 glia and astrocytes were identified and electrophysiologically characterized using the transgenic reporter mouse lines hGFAP-eGFP and Cx43-ki-eCFP, respectively. Functional responses to kainic acid (KA), activating AMPA/kainate receptors, and NMDA were assessed at the single-cell level.</p><p><strong>Results: </strong>KA evoked membrane current responses in the majority of NG2 glia, whereas NMDA responses were restricted to a smaller subset and were associated with the absence of A-type K+ currents. In passive astrocytes, approximately half of the cells responded to KA and NMDA. KA responses showed heterogeneous current patterns, including increased cationic conductance and, in a subset of cells, reduced outward K+ currents, whereas NMDA responses were comparatively homogeneous.</p><p><strong>Discussion: </strong>These findings demonstrate substantial functional heterogeneity of ionotropic glutamate receptor responses within established optic nerve glial populations. Glutamate responsiveness does not define distinct glial cell types but rather represents an additional functional feature within NG2 glia and astrocytes. This diversity may enable glial cells to adapt to local neuronal activity and contribute to axon-glia communication and white matter homeostasis.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1911068"},"PeriodicalIF":4.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024352","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":"Editorial: The roles of peripheral immune cells and their circulatory effector molecules in neuropsychiatric disorders, volume II.","authors":"Bernhard T Baune, Marie-Eve Tremblay, Karl Bechter, Li Tian","doi":"10.3389/fncel.2026.1976330","DOIUrl":"https://doi.org/10.3389/fncel.2026.1976330","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1976330"},"PeriodicalIF":4.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024367","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":"Kirrel3 homophilic adhesion function is required for male-directed aggression and vomeronasal acuity to urine chemosignals.","authors":"Sydney Fearnley, Neelima Vaddadi, Emilie Dumontier, Jean-François Cloutier","doi":"10.3389/fncel.2026.1926504","DOIUrl":"10.3389/fncel.2026.1926504","url":null,"abstract":"<p><p>The accessory olfactory system regulates social and reproductive behaviours in mice that are essential for survival. Proper function of this system depends on the accurate mapping of chemosensory information detected by vomeronasal sensory neurons (VSNs) into glomerular activation patterns. The formation of glomerular maps requires members of the Kirrel family of cell adhesion proteins, which mediate the coalescence of VSN axons into glomeruli. Disruption of Kirrel3 function, either through genetic deletion (<i>Kirrel3^-/-</i> ) or by impairing its homophilic interaction via a single amino acid substitution (<i>Kirrel3^Q128A</i> ), disrupts axonal glomerular map formation. Here, we compared the performance of the <i>Kirrel3^Q128A</i> mice to <i>Kirrel3^-/-</i> mice in behavioural assays involving social interactions. Similar to <i>Kirrel3^-/-</i> mice, <i>Kirrel3^Q128A</i> male mice exhibited reduced male-male aggression in the resident-intruder assay. Female <i>Kirrel3^Q128A</i> mice lacked maternal aggression, although other maternal behaviors, including pup retrieval and nesting, remained intact. Urine preference assays revealed increased detection thresholds to both male and female urine in <i>Kirrel3^Q128A</i> mice, indicating reduced vomeronasal sensitivity. However, response to non-social attractive and aversive odorants were unaffected. Notably, social novelty behavior was impaired in <i>Kirrel3^-/-</i> mice but preserved in <i>Kirrel3^Q128A</i> mice. Taken together, these results demonstrate that loss of Kirrel3-mediated adhesion is sufficient to recapitulate key deficits in vomeronasal function and VNO-dependent behaviors observed in Kirrel3 null mice, while selectively sparing certain aspects of social behavior.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1926504"},"PeriodicalIF":4.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024294","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":"The effects of abused drugs on ferroptosis pathways: potential therapeutic targets for substance use disorders.","authors":"Tamara Bouchard, Brooke Russell, Liam Liyang Guo, Tina Nguyen, Yan Cheng, Yan Y Sanders, Ming-Lei Guo","doi":"10.3389/fncel.2026.1899553","DOIUrl":"10.3389/fncel.2026.1899553","url":null,"abstract":"<p><p>Substance use disorders (<b>SUDs</b>) remain major public health concerns worldwide, particularly in developed countries. SUDs are characterized by persistent neuroinflammation and synaptic dysfunction in the brain. Despite decades of extensive investigation, the detailed mechanisms underlying SUDs remain elusive. Ferroptosis is a highly regulated cell death process deeply affected by iron metabolism, lipid peroxidation, reactive oxygen species (<b>ROS</b>) production, and antioxidant systems. It has been implicated in multiple neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ischemic stroke. Recently, emerging evidence has highlighted the role of ferroptosis in drug-induced pathological changes. Various types of abused substances including alcohol, cocaine, methamphetamine (<b>METH)</b> nicotine, cannabis, and opioids have been shown to disrupt ferroptosis-relevant pathways, leading to microglial activation and neuronal injury. Inhibition of ferroptosis could mitigate these pathological changes in preclinical models. Here, we summarize current evidence demonstrating the effects of abused drugs on ferroptosis pathways. Collectively, these findings underscore the potential role of ferroptosis in the pathophysiology of SUDs. Targeting ferroptosis may represent a promising therapeutic strategy for alleviating drug-induced neurological damage and improving recovery outcomes such as cognitive and memory deficiency in individuals with addiction.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1899553"},"PeriodicalIF":4.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13581560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988310","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":"BFP, bifacial weakness with paresthesias secondary to trauma: a case report.","authors":"Jingjing Chen, Xuxia Tang, Shuo Dai, Xiao He","doi":"10.3389/fncel.2026.1916633","DOIUrl":"10.3389/fncel.2026.1916633","url":null,"abstract":"<p><strong>Background: </strong>BFP, bifacial weakness with paresthesias is a rare variant of Guillain-Barré syndrome (GBS). Here, we detail the diagnosis and treatment process of a patient with BFP secondary to head trauma to highlight its importance.</p><p><strong>Case: </strong>A 47-year-old man presented with bilateral peripheral facial paralysis, hearing loss, and sensory impairment in both lower limbs following a car accident. Temporal bone fracture was first considered as the cause of facial palsy. We gave glucocorticoid therapy to the patient, but it was ineffective, facial nerve decompression surgery was planned as a consideration. However, diminished tendon reflexes was noted on the 12th day post-trauma, then cerebrospinal fluid (CSF) testing and anti-ganglioside antibodies were performed. Based on the medical history and Laboratory testing, the patient was diagnosed with BFP, a rare variant of GBS. Plasma exchange therapy was performed on the patient. At six-month follow-up, except for hearing loss, the other symptoms had almost returned to normal.</p><p><strong>Conclusion: </strong>In this article, we report a case of BFP secondary to head trauma. We emphasize that in patients with post-traumatic bilateral facial nerve paralysis, a comprehensive neurological examination is essential for accurate diagnosis and to avoid unnecessary medications or surgery.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1916633"},"PeriodicalIF":4.4,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13581528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988804","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":"Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.","authors":"Sania Sultana, Sougata Ray, Sarbani Samaddar, Sourav Banerjee","doi":"10.3389/fncel.2026.1883287","DOIUrl":"10.3389/fncel.2026.1883287","url":null,"abstract":"<p><p>Despite long-standing investigations into the neural and molecular correlates of memory, there persists a lack of comprehensive understanding of the cellular and subcellular processes that go awry in cases of neurodivergent and neuropathological phenotypes. While the mechanisms of memory encoding, consolidation, and retrieval are well-characterized in neurotypical models, disruptions in these processes often manifest as cognitive dysfunctions in the contexts of neurodevelopment and neurodegeneration. In this review, we specifically examine the molecular frameworks of memory processing arising from neurodevelopmental disorders. Given that developmental disorders affecting early stages of neural circuitry formation are manifested much later, in the adolescent or adult stages of life, it is important to delineate exactly how the molecular underpinnings of memory formation lead to atypical behavioral phenotypes manifested in different neurodevelopmental conditions. By integrating behavioral phenotypes with underlying circuit and molecular pathologies, this paper argues for a multiscale perspective to understand and address the divergence between neurotypical and neurodivergent memory function.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1883287"},"PeriodicalIF":4.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13576156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148976229","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":"Primary cell and tissue cultures of human choroid plexus epithelial cells.","authors":"Ronja Bihlmaier, Melanie Scharr, Peter H Neckel, Bernhard Hirt, Andreas F Mack","doi":"10.3389/fncel.2026.1827493","DOIUrl":"10.3389/fncel.2026.1827493","url":null,"abstract":"<p><p>Choroid plexus epithelial cells (CPEC) are implicated in cerebrospinal fluid (CSF) production and the site of the inner blood-cerebrospinal fluid barrier. CPEC are specialized ependymal cells with characteristic cell junctions, intermediate filaments, and transport protein expression, including aquaporins. We have recently found that, in addition to aquaporin-1, a subset of CPEC in the human brain express aquaporin-4 (AQP4), the main water channel in the brain that has been implicated in water homeostasis and glymphatic system function. We therefore aimed to establish primary cultures from human CP to study AQP4 expression. We collected CP tissue from human body donors <i>post mortem</i> to grow CPEC <i>in vitro</i>. We successfully established two primary culture models for human CP tissue. In an organ culture model, small pieces of CP tissue were explanted on PTFE membranes. In a second model, cells from CP were dissociated and seeded on either laminin or collagen substrate. We monitored cell and tissue growth and investigated protein expression by immunofluorescence. Tissue integrity of explant cultures was maintained throughout the cultivation period of several weeks. Immunofluorescence signals for zonula occludens protein-1 (ZO1), AQP1, and Na/K-ATPase were present although the expression patterns became increasingly irregular and non-polar over time. In dissociation cultures, cells attached and grew very slowly initially but reached confluency after several weeks. Cultures were passaged up to 6 times and could be cryopreserved. Application of cytosine arabinoside suppressed the growth of macrophages and most likely fibroblasts. These primary dissociation cultures were identified as epithelial by their morphology and positive immunofluorescence for transthyretin, vimentin. Na/K-ATPase, ZO-1, cytokeratin, and AQP1. In both culture models, cells expressed AQP4. In dissociation cultures, AQP4 appeared to colocalize with ZO-1 at cell-cell contact sites in many CPEC but showed separate localizations at high resolution. These studies show that primary organ and cell cultures can be generated from human <i>post mortem</i> CP tissue suitable to investigate regulation and localization of AQP4. Together, these culture models provide valuable tools to investigate the proteins involved in CSF production and glymphatic clearance, relevant for the pathogenesis of neurodegenerative diseases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1827493"},"PeriodicalIF":4.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967473","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":"Editorial: Cellular and animal models of neurodegenerative and neuroinflammatory conditions.","authors":"Juan Antonio García-León, Beatriz García-Díaz, David Baglietto-Vargas, Carlos J Rodriguez-Ortiz","doi":"10.3389/fncel.2026.1961369","DOIUrl":"https://doi.org/10.3389/fncel.2026.1961369","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1961369"},"PeriodicalIF":4.4,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13572680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967458","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":"The research landscape of ferroptosis in ischemic stroke: a bibliometric analysis of the literature from 2017 to 2025 based on the WOS and PubMed databases.","authors":"Hongmei Tang, Yujie Zhang, Mingxia Zhang, Jia Hu, Lingxue Wang, Shuangyang Li, Yuting Pu, Xue Bai","doi":"10.3389/fncel.2026.1836830","DOIUrl":"10.3389/fncel.2026.1836830","url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke is a leading cause of disability and mortality worldwide. Ferroptosis-an iron-dependent, lipid peroxidation-driven programmed cell death-has emerged as a key contributor to post-stroke neuronal injury, with research expanding rapidly since 2017.</p><p><strong>Objective: </strong>This study employs bibliometric methods to systematically analyze literature on ferroptosis in ischemic stroke from 2017 to 2025, aiming to elucidate the field's development trajectory, research hotspots, emerging frontiers, and collaborative networks.</p><p><strong>Methods: </strong>Data were retrieved from the Web of Science Core Collection and PubMed, limited to English articles and reviews published between 2017 and 2025. For PubMed, an additional search was conducted to capture empirical studies on ferroptosis inhibitors. Bibliometric analyses were performed using VOSviewer, CiteSpace, and Bibliometrix R package.</p><p><strong>Results: </strong>A total of 646 WoS-indexed articles were analyzed. Annual publication output showed exponential growth. China, the United States, and India led in publication volume, with China accounting for over half of global output; international collaboration centered on China-US partnerships. Research hotspots focused on molecular mechanisms (GPX4, System Xc^-, Nrf2/HO-1), key regulators (ACSL4, FSP1), and therapeutic strategies (ferroptosis inhibitors, natural compounds). Analysis of 64 PubMed-indexed studies on ferroptosis inhibitors revealed that China also dominated this area, with the National Natural Science Foundation of China as the primary funding source. Emerging frontiers indicate a shift from mechanistic studies toward clinical translation, including biomarker development, nano-targeted delivery, and neurovascular unit protection.</p><p><strong>Conclusion: </strong>From 2017 to 2025, research on ferroptosis in ischemic stroke has rapidly evolved from concept introduction and mechanistic exploration toward clinical translation. Bibliometric analysis delineates a clear trajectory and evolving knowledge framework. Future research will likely emphasize interdisciplinary integration, clinical translation, and personalized therapeutic strategies.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1836830"},"PeriodicalIF":4.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918849","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":"Integrative transcriptomic- neuroimaging analysis reveals polygenic correlates of interhemispheric functional decoupling in ischemic stroke.","authors":"Ri-Bo Chen, Yu-Xuan He, Xin Huang, Chang Wang","doi":"10.3389/fncel.2026.1908231","DOIUrl":"10.3389/fncel.2026.1908231","url":null,"abstract":"<p><strong>Background: </strong>Functional magnetic resonance imaging (fMRI) has revealed abnormal brain activity patterns in stroke patients, yet the genetic correlates underlying functional homotopy - defined as synchronized spontaneous activity between bilateral homologous brain regions - remain poorly characterized. This study investigates the genetic basis of voxel-mirrored homotopic connectivity (VMHC) abnormalities in stroke patients.</p><p><strong>Methods: </strong>We analyzed resting-state fMRI data from 50 stroke patients and 50 healthy controls (HC) to quantify VMHC. Spatial transcriptome-neuroimaging correlations were established using the Allen Human Brain Atlas (AHBA) to identify VMHC-associated genes. Transcriptomic analyses combined pathway-centric functional annotation (DAVID) with protein-protein interaction (PPI) network modeling (STRING v12.0).</p><p><strong>Results: </strong>Stroke patients exhibited significantly reduced VMHC in the rectus gyrus, superior temporal gyrus, middle occipital gyrus, cuneus, and right calcarine/left posterior cingulate gyrus (<i>p</i> < 0.05, GRF-corrected). VMHC alterations correlated positively and negatively with 1,198 genes each. Transcriptomic profiling revealed significant enrichment in synaptic vesicle trafficking, mitochondrial energy metabolism, and neuroinflammation-related pathways. PPI mapping uncovered multi-tiered networks with hub genes including <i>BRCA1</i>, <i>CDK9</i>, <i>ACTB</i>, and <i>ATP6V1A/F</i> involved in transcriptional regulation, cytoskeletal dynamics, and vesicular acidification.</p><p><strong>Conclusion: </strong>This multimodal integration study elucidates polygenic correlates of post-stroke VMHC abnormalities, demonstrating that interhemispheric coordination may depend on synergistic interactions among functionally diverse gene clusters. Our findings provide a molecular framework for understanding post-stroke neural network reorganization and offer a link between functional neuroimaging phenotypes and gene expression, though all associations remain correlational and require mechanistic validation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1908231"},"PeriodicalIF":4.4,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918854","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}