Frontiers in Cellular Neuroscience最新文献

{"title":"Cholinergic input origins and current response properties in rat interstitial nucleus of Cajal neurons.","authors":"Taketoshi Sugimura, Yasuhiko Saito","doi":"10.3389/fncel.2026.1925102","DOIUrl":"https://doi.org/10.3389/fncel.2026.1925102","url":null,"abstract":"<p><p>The interstitial nucleus of Cajal (INC) and the prepositus hypoglossi nucleus (PHN) function as the neural integrators for vertical and horizontal gaze holding, respectively. Previous studies have suggested that cholinergic inputs from the mesopontine tegmentum modulate the function of the horizontal integrator; however, the modulation properties and origins of cholinergic inputs in the vertical integrator remain unclear. In this study, we investigated the cholinergic responses of INC neurons and the anatomical origin of the cholinergic inputs in rats. Whole-cell recordings in brainstem slices revealed that local application of acetylcholine (ACh) induced inward currents in INC neurons mediated by both nicotinic and muscarinic ACh receptors (nAChRs and mAChRs). Although current responses were predominantly mediated by nAChRs in PHN neurons, the participation of nAChRs and mAChRs differed depending on the INC neuron type. Retrograde tracing using an adeno-associated virus (AAV) in choline acetyltransferase (ChAT)-tdTomato transgenic rats demonstrated that the primary origin of cholinergic inputs to the INC was the caudal magnocellular region of the medial vestibular nucleus (MVeMC). Furthermore, the primary cholinergic inputs to the PHN originated from both the caudal MVeMC and the caudal PHN itself. These results indicate that the vertical neural integrator shares a common cholinergic source in the caudal MVN with the horizontal integrator, although the relative contributions of nAChRs and mAChRs are not necessarily shared between INC and PHN neurons. These findings suggest a potential role for cholinergic modulation in both vertical and horizontal gaze holding.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1925102"},"PeriodicalIF":4.4,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13739500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149370260","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":"Retraction: Effects of bone marrow mesenchymal stem cells (BM-MSCs) on rat pial microvascular remodeling after transient middle cerebral artery occlusion.","authors":"","doi":"10.3389/fncel.2026.2026327","DOIUrl":"https://doi.org/10.3389/fncel.2026.2026327","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3389/fncel.2015.00329.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"2026327"},"PeriodicalIF":4.4,"publicationDate":"2026-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13742250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149370261","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":"Adeno-associated virus gene delivery targeting corneal-projecting trigeminal ganglion neurons.","authors":"Samuel S Reynolds, Md Zeeshan Rasheed, Ken Niyonkuru, Sachin Parikh, Kyle Whyland, Brooklynn M Merrill, William Perez, Sreya Mitra, Tomasz Zal, Hongmin Yun, Brian Davis, Anthony J St Leger, Anna Matynia, Ian D Meng","doi":"10.3389/fncel.2026.1925806","DOIUrl":"10.3389/fncel.2026.1925806","url":null,"abstract":"<p><p>Corneal innervation is essential for ocular surface homeostasis and protection, yet methods for selectively labeling and manipulating cornea-projecting neurons remain limited. Conventional retrograde tracers can identify cornea-projecting cell bodies in the trigeminal ganglion (TG), but they do not enable the expression of genetically encoded effector proteins, sensors, or recombinases. We describe and validate intrastromal adeno-associated virus (AAV) delivery as an approach for labeling cornea-projecting TG neurons in mice. A 1-2-μL viral injection was delivered into the corneal stroma and labeling was assessed 2-12 weeks later in cleared whole TG, TG sections, corneal whole mounts, and thick brainstem sections. Multiple AAV vectors, including tdTomato-, eGFP-, or mCherry-expressing vectors and Cre-expressing vectors in Ai14 tdTomato reporter mice, produced consistent neuronal labeling concentrated in the dorsomedial ophthalmic division of the TG. Native tdTomato fluorescence was readily detected, and eGFP labeling could be enhanced using immunolabeling with fluorophore-enhancing antibodies, increasing detection of labeled somata and axonal fibers. AAV-mediated labeling in the TG substantially overlapped with WGA and Fast Blue tracing from the cornea, although AAV labeled fewer neurons overall. Cre-expressing AAV vectors activated reporter expression in Ai14 mice, demonstrating compatibility with transgenic reporter strategies. Labeled axons were visualized at both peripheral and central projection sites. At the ocular surface, reporter expression was correlated to the extent of neuronal transduction. Central projections were observed in subnucleus principalis, the interpolaris/caudalis transition zone, and caudal subnucleus caudalis extending into upper cervical spinal cord. AAV transduction resulted in no gross immune activation. These findings indicate that intrastromal AAV delivery provides a versatile approach for anatomical tracing and genetic access to cornea-projecting neurons, enabling expression of genetically encoded tools for optogenetic and chemogenetic control, activity monitoring, and targeted genetic manipulation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1925806"},"PeriodicalIF":4.4,"publicationDate":"2026-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13735549/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149341462","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":"Impaired Kv4.2-DPP6 complex dynamics in a mouse model of Angelman syndrome.","authors":"Jia-Hua Hu, Ying Liu, Cole Malloy, Dax A Hoffman","doi":"10.3389/fncel.2026.1953686","DOIUrl":"10.3389/fncel.2026.1953686","url":null,"abstract":"<p><strong>Introduction: </strong>Angelman syndrome (AS) is a neurodevelopmental disorder caused by loss of neuronal expression of the E3 ubiquitin ligase UBE3A and is associated with altered neuronal excitability. We previously identified the dendritic A-type K+ channel subunit Kv4.2 as an activity-dependent substrate of UBE3A. However, where UBE3A interacts with Kv4.2 during activity-dependent trafficking and how this pathway regulates Kv4.2 channel complexes and dendritic distribution remain unclear..</p><p><strong>Methods: </strong>We combined live-cell bungarotoxin labeling and biochemical surface-labeling approaches to examine UBE3A association with surface-derived Kv4.2. Co-immunoprecipitation and immunoblotting were used to assess Kv4.2 association with the auxiliary subunit DPP6 and activity-dependent Kv4.2 phosphorylation in wild-type (WT), UBE3A-deficient (AS), and DPP6 knockout (KO) mice. Kv4.2 immunostaining and quantitative line-scan analysis were used to examine its proximal-to-distal distribution in hippocampal CA1 dendrites.</p><p><strong>Results: </strong>UBE3A preferentially associated with internalized rather than surface-resident Kv4.2, supporting a post-endocytic site of UBE3A action. In AS mice, Kv4.2-DPP6 association was reduced and failed to undergo further activity-dependent remodeling following pentylenetetrazole (PTZ)-induced seizures, despite unchanged DPP6 expression and preserved basal Kv4.2 phosphorylation. In contrast, DPP6 deficiency increased basal Kv4.2 phosphorylation at T602 and T607 and disrupted its activity-dependent phosphorylation dynamics, indicating reciprocal regulation between Kv4.2 phosphorylation and DPP6 association. DPP6KO mice exhibited impaired Kv4.2 gradients along both apical and basal CA1 dendrites. Similarly, AS mice showed impaired dendritic Kv4.2 gradients and reduced activity-dependent redistribution following kainic acid-induced seizures.</p><p><strong>Conclusion: </strong>These findings support a model in which neuronal activity promotes remodeling and internalization of Kv4.2-containing channel complexes, followed by UBE3A-dependent processing of the post-endocytic Kv4.2 pool. Loss of UBE3A disrupts Kv4.2-DPP6 complex dynamics and dendritic Kv4.2 organization, thereby reducing the capacity for activity-dependent channel redistribution. These results identify UBE3A as an important regulator of Kv4.2 homeostasis and provide a mechanistic link between UBE3A deficiency, altered dendritic ion-channel organization, and neuronal dysfunction in Angelman syndrome.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1953686"},"PeriodicalIF":4.4,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13730888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149333210","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":"An age-related decline in human fluid intelligence corresponds with immature astroglia prevalence.","authors":"Aswathy Ammothumkandy, Luis Corona, Nadia A Atai, Aidin Abedi, Nora Jimenez, Michelle Armacost, Lina M D'Orazio, Virginia Zuverza-Chavarria, Alisha Cayce, Mohammad Shariq, Ryan McGinn, Darrin Lee, Brian Lee, Christianne Heck, Jonathan J Russin, Charles Y Liu, Jason A D Smith, Michael A Bonaguidi","doi":"10.3389/fncel.2026.1926804","DOIUrl":"10.3389/fncel.2026.1926804","url":null,"abstract":"<p><p>Age-related cognitive decline remains a daunting health challenge, and targeting neuronal cells alone has been insufficient to halt its progression. Astroglia are emerging as key players in cognitive function and dysfunction, yet their relevance to age-associated cognitive decline in humans remains unclear. Epilepsy patients undergo age-amplified progressive cognitive decline. Our prior research in Mesial Temporal Lobe Epilepsy (MTLE) patients identified pathological stellar Dcx + immature astroglia in epileptic, but not healthy hippocampus. In this study, we combined histology data with pre-surgical neuropsychology tests to assess (1) age-associated cognitive decline in MTLE patients (<i>N</i> = 40), (2) age-related changes in Dcx + immature astroglia (<i>N</i> = 29), and (3) the association between Dcx + immature astroglia and cognitive decline (<i>N</i> = 19). We observed a strong decline in fluid intelligence, visuospatial reconstruction, and memory with age. An increase in Dcx + immature astroglia positively correlated with age, whereas negatively associated with nonverbal abstract reasoning and fluid intelligence as measured by the Raven's Progressive Matrices test. These findings reveal an interplay among aging, fluid intelligence decline, and immature astroglia prevalence in epilepsy patients. Our study suggests immature astroglia represent a new cellular target to consider for altering age-associated cognitive decline.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1926804"},"PeriodicalIF":4.4,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13727376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149319612","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":"Case Report: Sporadic Creutzfeldt-Jakob disease initially misdiagnosed as ischemic stroke: a diagnostic challenge and biomarker-based clarification.","authors":"Wenjie Hao, Xuan Zhou, Meixia Wang, Wenming Yang, Ting Cheng","doi":"10.3389/fncel.2026.1938627","DOIUrl":"10.3389/fncel.2026.1938627","url":null,"abstract":"<p><strong>Background: </strong>Sporadic Creutzfeldt-Jakob disease (sCJD) is a rare and uniformly fatal prion disorder characterized by rapidly progressive dementia and heterogeneous neurological manifestations. Early sCJD may be misinterpreted as cerebrovascular disease, particularly when focal neurological deficits, unilateral diffusion abnormalities, and vascular risk factors coexist.</p><p><strong>Case presentation: </strong>We report a 76-year-old man with a history of hypertension who initially presented with dizziness and gait instability, followed by progressive right-sided weakness, and was initially diagnosed with ischemic stroke in the setting of intracranial arterial stenosis. Despite antiplatelet and vascular management, the patient experienced rapid cognitive decline, psychiatric disturbances, aphasia, and progressive hemiparesis. Follow-up MRI demonstrated progressive, non-territorial cortical ribbon-like diffusion restriction predominantly involving the left insular, parietal, frontal, and temporal cortices. CSF analysis revealed markedly elevated total tau (4553.50 pg/mL; laboratory-reported cutoff: < 399 pg/mL), phosphorylated tau (66.93 pg/mL; laboratory-reported cutoff: < 50 pg/mL), and 14-3-3γ protein (50515 AU/mL; laboratory-reported cutoff: < 20,000 AU/mL). Autoimmune encephalitis antibodies and metagenomic next-generation sequencing were negative. PRNP genetic testing detected no pathogenic variant in the patient and his son. EEG showed diffuse slowing without periodic sharp wave complexes. According to the 2017 International CJD Surveillance Network criteria, the diagnosis was classified as probable sCJD on the basis of rapidly progressive cognitive impairment, two clinical features (documented cerebellar ataxia and pyramidal signs), characteristic MRI abnormalities, and positive CSF 14-3-3; the typical EEG criterion was absent and RT-QuIC was not performed.</p><p><strong>Conclusion: </strong>This case highlights the diagnostic challenge of early sCJD initially misdiagnosed as ischemic stroke in the presence of coexisting vascular pathology. Recognition of non-vascular diffusion patterns, careful reassessment of atypical clinical progression, and adjunctive CSF biomarker assessment may facilitate timely diagnostic reconsideration and help avoid unnecessary interventions.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1938627"},"PeriodicalIF":4.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149295665","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":"Tissue-resident and recruited mononuclear phagocyte organization in the cochlea under homeostasis and implant-induced inflammation.","authors":"Shakila Mahmuda Fatima, Muhammad Taifur Rahman, Brian J Mostaert, Ibrahim Razu, Bryce Hunger, Shanta Afrin, Sharar Naiarin Haque, Nashwaan Ali Khan, Zhenshen Zhang, Alexander D Claussen, Marlan R Hansen","doi":"10.3389/fncel.2026.1895870","DOIUrl":"10.3389/fncel.2026.1895870","url":null,"abstract":"<p><strong>Background: </strong>The cochlea contains a diverse population of immune cells that contribute to tissue homeostasis and to responses to injury. Among these, mononuclear phagocytes including tissue-resident macrophages, dendritic cells, and microglia-like cells play central roles in immune surveillance and inflammation. Cochlear implantation induces a robust foreign body response, and here we sought to map the spatial distribution of mononuclear phagocytes across distinct cochlear compartments in healthy cochleae and following implantation.</p><p><strong>Materials and methods: </strong>We used two reporter mice in this study: C57BL/6-Tmem119em2Gfng/J (TMEM119+/GFP as reporter for microglia), B6. FVB-1700016L21RikTg (Itgax-DTR/EGFP)57Lan/J (CD11c+/GFP as reporter for dendritic cells). To define the spatial organization of different types of mononuclear phagocytes in normal cochleae and after implantation, 30-μm mid-modiolar cochlear sections from these reporter mice were imaged using a confocal microscope. Immunolabeling with cell-specific and activation markers was used to further characterize the cellular distributions and responses.</p><p><strong>Results: </strong>We identify heterogeneous distribution of mononuclear phagocytes throughout the cochlea. CD11c-positive dendritic cells display a more restricted baseline distribution, residing primarily in Rosenthal's canal and the spiral ligament; they selectively accumulate at the implant-tissue interface in the scala tympani after implantation and upregulate major histocompatibility complex class II expression, consistent with antigen-presenting phenotypes. In addition, expression of microglia-associated markers, including TMEM119 and P2Y12, identifies a microglia-like population within specific cochlear sub-regions that persists following implantation.</p><p><strong>Conclusion: </strong>Together, these findings reveal an immune landscape in the cochlea under both healthy and implant-associated inflammatory conditions. CD11c-positive dendritic cells appear to play a central role in the inflammatory response to cochlear implants, becoming activated and localizing to the interface with the biomaterial surface.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1895870"},"PeriodicalIF":4.4,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13719395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149295671","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":"Neuron myelination is accelerated by Bruton's tyrosine kinase inhibition via microglial extracellular vesicles.","authors":"Matteo Tartaglia, Arianna Ioni, Mariassunta De Luca, Laura Vilardo, Igea D'Agnano, Antonella Conte, Cristina Limatola, Myriam Catalano","doi":"10.3389/fncel.2026.1864654","DOIUrl":"https://doi.org/10.3389/fncel.2026.1864654","url":null,"abstract":"<p><strong>Introduction: </strong>The altered myelin repair observed in demyelinating diseases such as multiple sclerosis (MS) potentially exposes axons to various stressors, with consequent neurodegeneration. Preclinical evidence has demonstrated that Bruton's tyrosine kinase inhibitors (BTKi), such as ibrutinib, delay MS progression by acting on myeloid cells.</p><p><strong>Methods: </strong>We investigated the effects of ibrutinib on remyelination using a novel in vitro model of spinal cord neurons derived from postnatal mice.</p><p><strong>Results: </strong>We demonstrated that (1) spinal cord neuron cells represent a suitable model for investigating myelination following L‑α‑lysophosphatidylcholine (LPC) treatment; (2) ibrutinib induces remyelination and reduces stathmin‑1 expression in spinal cord cultures; and (3) ibrutinib reduces the inflammatory phenotype of microglia‑like BV2 cells, thereby modulating the expression of miR‑223 in extracellular vesicles (EVs).</p><p><strong>Discussion: </strong>Altogether, these data pave the way for a better understanding of the mechanisms underlying remyelination following ibrutinib treatment and support the hypothesis that EV‑derived microglial cells play a key role.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1864654"},"PeriodicalIF":4.4,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149295739","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 role of cellular subtypes in striatal activity.","authors":"Elodie Fino, Maxime Assous, Marc Vincent Fuccillo","doi":"10.3389/fncel.2026.2010201","DOIUrl":"https://doi.org/10.3389/fncel.2026.2010201","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"2010201"},"PeriodicalIF":4.4,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13713365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149295736","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":"Serotonergic regulation of neuronal excitability and glutamatergic synaptic transmission in rat claustrum.","authors":"Renee Rouleau, Saida Oubraim, Lizemarie Cirone, Roh-Yu Shen, Samir Haj-Dahmane","doi":"10.3389/fncel.2026.1951375","DOIUrl":"10.3389/fncel.2026.1951375","url":null,"abstract":"<p><p>The claustrum (CLA) receives dense serotonergic innervation from dorsal raphe nucleus (DRN) serotonin (5-HT) neurons, which are implicated in regulating sleep and stress homeostasis. However, the mechanisms by which 5-HT regulates the excitability of CLA neurons remain poorly defined. In the present study, we combined whole-cell patch-clamp recordings, 5-HT uncaging, and receptor pharmacology to examine the effects of 5-HT on the excitability of CLA neurons and their glutamatergic synapses. We found that 5-HT consistently induced membrane hyperpolarization or depolarization in regular-spiking type I and type II neurons, whereas it predominantly induced hyperpolarization in strongly adapting CLA neurons. The 5-HT-induced membrane hyperpolarization and depolarization were mediated by 5-HT1A receptors (5-HT1ARs) and 5-HT2A receptors (5-HT2ARs), respectively. Furthermore, we showed that activation of presynaptic 5-HT2ARs inhibits glutamatergic synaptic transmission in the CLA by reducing glutamate release. This effect was not mediated by the canonical phospholipase C (PLC) signaling cascade. Collectively, these findings reveal cell type-specific and multifaceted serotonergic modulation of the intrinsic excitability and synaptic transmission in the claustrum.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1951375"},"PeriodicalIF":4.4,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13710022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149286011","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}