Journal of Neurochemistry最新文献

{"title":"Estradiol Replacement Modulates Synaptic Transmission-Related Proteins in the Hippocampus of Ovariectomized Rats: An Exploratory Proteomic Approach","authors":"Amanda Paula Pedroso,&nbsp;Adriana Pereira Souza,&nbsp;Guilherme Araújo Câmara,&nbsp;Meira Maria Forcellini Machado,&nbsp;Valter Tadeu Boldarine,&nbsp;Lila Missae Oyama,&nbsp;Mônica Marques Telles,&nbsp;Alexandre Keiji Tashima,&nbsp;Eliane Beraldi Ribeiro","doi":"10.1111/jnc.70536","DOIUrl":"https://doi.org/10.1111/jnc.70536","url":null,"abstract":"<p>The loss of ovarian hormones in postmenopause influences cognition, emotion and energy homeostasis, processes integrated by the hippocampus. The mechanisms by which estradiol influences this area have not been fully understood. The present study aimed at investigating the effects of estradiol on the rat hippocampus proteome of ovariectomy-induced menopause either followed by estradiol replacement or not. Eighteen 3-month-old female Wistar rats were either ovariectomized or sham operated and fed with standard chow for 3 months. A subgroup of ovariectomized rats received estradiol replacement. The hippocampi were processed using data independent acquisition MS-based proteomics and differentially expressed proteins were submitted to bioinformatics analysis for a pathway-based functional understanding of the estradiol effects. Proteomic analysis revealed that 49 hippocampal proteins were modulated by ovariectomy and estradiol replacement. Functional analysis of the differentially expressed proteins revealed the enrichment of terms related to energy metabolism (comprising glycolysis/gluconeogenesis, pyruvate metabolism, oxidative phosphorylation, and response to oxidative stress) and neuron projection (comprising cytoskeleton organization, regulation of vesicle-mediated transport, and modulation of chemical synaptic transmission). The present dataset indicates that, at the hippocampus, estradiol affects mitochondrial dynamics, lipid metabolism and intracellular trafficking machinery and influences dendritic and synaptic transmission and brain plasticity. Some alterations observed in proteins have not yet been described in the hippocampus in the context of menopause and estradiol replacement. These data provide new insights into the mechanisms involved with menopause effects and may help future studies related to drug development for the prevention and treatment of postmenopause associated symptoms.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70536","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753655","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":"Distinct Adrenal Medulla Activity in Germ-Free Versus Conventional Male Rats Under Acute and Chronic Stress","authors":"Camille Etienne,&nbsp;Claire Bernat,&nbsp;Magali Monnoye,&nbsp;Virginie Andry,&nbsp;Catherine Philippe,&nbsp;Claire Maudet,&nbsp;Elise Maximin,&nbsp;Laurent Naudon,&nbsp;Yannick Goumon,&nbsp;Christine Heberden,&nbsp;Nathalie C. Guérineau,&nbsp;Sylvie Rabot","doi":"10.1111/jnc.70538","DOIUrl":"https://doi.org/10.1111/jnc.70538","url":null,"abstract":"<p>It has now been well established that gut microbiota significantly influences emotional and neuroendocrine responses to stress. Specifically, multiple pieces of evidence from various preclinical models indicate that gut microbiota regulates the response of the hypothalamic–pituitary-adrenocortical (HPA) axis to acute and chronic stress. In contrast, the influence of gut microbiota on the adrenomedullary tissue, which is responsible for the production and release of catecholamines—the first hormones released in response to stress—has received little attention. Therefore, our study aimed to explore whether adrenal corticosterone and catecholamine biosynthesis were differently regulated in germ-free (GF) and conventional, specific pathogen-free (SPF) male rats when exposed to unpredictable chronic mild stress, acute metabolic stress, or both. Results showed that both GF and SPF chronically stressed rats had significantly (<i>p</i> &lt; 0.05) heavier adrenal glands (+30% for GF, +21% for SPF) compared to unstressed animals. Gene expression levels of corticosterone biosynthesis enzymes and plasma and adrenal corticosterone concentrations did not differ significantly between control rats and those exposed to chronic, acute, or both stress factors, whether in GF or SPF rats. The same result was observed for the genes encoding tyrosine hydroxylase and dopamine β-hydroxylase, two enzymes involved in catecholamine biosynthesis. By contrast, GF rats exhibited a 2.3-fold increase (<i>p</i> = 0.0271) in <i>Pnmt</i> gene expression (which encodes phenylethanolamine N-methyltransferase, the enzyme responsible for converting norepinephrine to epinephrine) and a 2.6-fold increase (<i>p</i> = 0.0786) in epinephrine concentration in the adrenal glands under combined stress conditions. This response was not observed in SPF rats. In these animals, chronic stress was found to reshape the composition and metabolic functions of the gut microbiota. Interestingly, this was accompanied by a 40% decrease in norepinephrine (<i>p</i> = 0.0364) and epinephrine (<i>p</i> = 0.0840) concentrations in their adrenal glands. This study highlights the gut microbiota as a regulator of adrenomedullary activity, enhancing our understanding of the interaction between peripheral and central stress circuitry.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70538","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753654","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":"Calcium-Dependent Cytoskeletal Collapse and Recovery of Axons After Partial Laser Ablation","authors":"Ashish Mishra,&nbsp;Pooja Joshi,&nbsp;Md Arsalan Ashraf,&nbsp;Pramod Pullarkat","doi":"10.1111/jnc.70539","DOIUrl":"10.1111/jnc.70539","url":null,"abstract":"<div>\u0000 \u0000 <p>Traumatic stretch or crush injury to axons causes widespread and often irreversible damage to the axonal cytoskeleton, in which calcium-mediated breakdown is known to play a central role. Unlike complete transection, where recovery must proceed through formation of a new growth cone, milder injury can disrupt the axonal cytoskeleton while leaving the plasma membrane intact. How the cytoskeleton fails, and how it can recover, under these conditions remains unclear. Here we address this using a partial laser-ablation method that damages the cytoskeleton and evokes a calcium transient while preserving membrane continuity. We show that the ensuing cytoskeletal retraction is set by a mechanical balance between acto-myosin contractility and microtubule stability: stabilizing microtubules or inhibiting acto-myosin contractility suppresses retraction. Moreover, chelating extracellular calcium mitigates degeneration and, in a subset of axons, permits complete recovery. We also show that microtubules and actin filaments show distinct loss and recovery dynamics and provide a hypothesis for the “burning-fuse” -like depolymerization of the microtubule bundle. These findings provide insights into how the axonal cytoskeleton collapses and recovers after injury and suggest strategies for mitigating damage.</p>\u0000 <p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Illuminating the Future of Catecholamine Detection","authors":"Julia Ackermann,&nbsp;Andreas Reiner,&nbsp;Sebastian Kruss","doi":"10.1111/jnc.70535","DOIUrl":"10.1111/jnc.70535","url":null,"abstract":"<p>Catecholamines such as dopamine (DA) and norepinephrine (NE) are critical neuromodulators which influence a wide range of physiological and behavioral processes. Optical sensors/probes are powerful tools to detect catecholamines with high spatial and temporal resolution, enabling real-time imaging in complex biological environments. In this review, we highlight recent advances in single-walled carbon nanotube (SWCNT) sensors and genetically encoded sensors for fluorescence-based catecholamine detection. We illustrate how these technologies have enabled new biological discoveries by allowing the spatiotemporal mapping of catecholamine release dynamics with unprecedented resolution. We discuss the complementary features of these techniques and remaining key challenges including molecular selectivity, tailored kinetics, and enhanced tissue penetration. Finally, we outline future directions and opportunities for integrating these technologies into neuroscience research, aiming to expand our understanding of catecholaminergic signaling across scales.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700814","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":"Microtubules in Spinal Cord Injury: From Cytoskeletal Dysregulation to Therapeutic Regeneration","authors":"Itzhak Fischer,&nbsp;Peter W. Baas","doi":"10.1111/jnc.70537","DOIUrl":"10.1111/jnc.70537","url":null,"abstract":"<p>Spinal cord injury (SCI) triggers an immediate and sustained disruption of the composition and organization of the neuronal cytoskeleton. Radical alterations in axonal and dendritic microtubules characterize both the acute injury phase and the protracted recovery period. For decades, researchers have sought to correct these microtubule defects as a therapeutic strategy to encourage axonal regeneration, collateral sprouting, and the functional rewiring of neuronal circuits. Recent studies have demonstrated that taxol and related microtubule-active drugs improve outcomes in rodent models. These benefits are achieved by preventing microtubule depolymerization, stabilizing existing polymers, and promoting new assembly within both afflicted neurons and the glial cells essential for repair. While these findings highlight the therapeutic potential of microtubule-based interventions, we posit that successful clinical translation necessitates a more sophisticated approach rooted in the growing knowledge of microtubule-related proteins and their intricate regulatory mechanisms. This review evaluates progress in this arena, specifically examining the microtubule interactome network that includes structural microtubule-associated proteins (MAPs) such as Tau, MAP1A, MAP1B, MAP2, and MAP6, as well as the stathmin family, plus-end tracking proteins, and microtubule-severing proteins such as fidgetin and spastin. In addition, we analyze the contribution of molecular motor proteins and regulatory MAPs, including CRMP2 and CRMP4, as well as upstream transcription factors governing their expression. Finally, we address convergent regulation through kinases such as GSK3β and CDK5, which represent a central mechanistic axis linking injury signaling to cytoskeletal failure. By integrating data from studies on development and regeneration into a unified mechanistic model, we provide a framework for microtubule-based therapeutics for SCI.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13447711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684922","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":"Complex Contributions of Methylglyoxal to Pain, Axon Degeneration, and Diabetic Peripheral Neuropathy","authors":"Gentry Totta-Griese,&nbsp;Douglas E. Wright","doi":"10.1111/jnc.70529","DOIUrl":"10.1111/jnc.70529","url":null,"abstract":"<p>Methylglyoxal is a highly reactive by-product of glycolysis that is elevated in diabetes and contributes to the development of diabetic peripheral neuropathy (DPN). DPN is characterized by nerve degeneration, typically manifesting in patients' extremities. This leads to patients experiencing numbness, burning, and pain. It has been established that elevated methylglyoxal levels lead to nociception, but the broader cellular effects of methylglyoxal on neurons in the dorsal root ganglia (DRG) remain poorly understood. This review provides mechanistic insight regarding methylglyoxal's impact on various cell types and disease contexts. Five main mechanisms were identified: protein glycation, proteostasis change, oxidative stress, metabolic changes, and increased inflammation. These mechanisms are thoroughly interconnected, contributing to cellular dysfunction associated with DPN. We propose that methylglyoxal functions as a central mediator in cellular stress, linking hyperglycemia and elevated glycolysis to neuronal dysfunction in DPN. There is extensive evidence that these mechanisms are methylglyoxal-driven in other cell types and diseases, but a gap in the field remains in determining whether and how they occur in DRG neurons. This is particularly important, as DPN is a frequent comorbidity in diabetes and metabolic diseases and greatly affects patients' quality of life. Understanding the effect of methylglyoxal on DRG in relation to these mechanisms will provide novel insights into the development of DPN and lead to new therapeutic targets.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669873","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":"Curving Actin Across Systems: Do Axonal Actin Rings Share Common Underlying Mechanisms?","authors":"Ana Rita Costa,&nbsp;Luís P. Rodrigues,&nbsp;Monica M. Sousa","doi":"10.1111/jnc.70534","DOIUrl":"https://doi.org/10.1111/jnc.70534","url":null,"abstract":"<p>Actin polymerization into curved and ring-shaped structures is an evolutionarily conserved mechanism that cells use to generate force, transmit tension, and maintain membrane architecture. In neurons, super-resolution imaging has revealed a striking periodic submembranous scaffold in axons, composed of circumferential actin rings interconnected by spectrin tetramers, known as the membrane periodic skeleton (MPS). This structure is widely conserved across species and neuronal subtypes and contributes to axonal integrity by reinforcing mechanical stability, organizing membrane proteins, regulating endocytosis, modulating axon caliber, and providing a transient platform for signaling. Although significant progress has been made in defining MPS functions, the molecular mechanisms governing the nucleation, assembly, and maintenance of axonal actin rings remain poorly understood. Here, we explore actin ring formation through comparison with three mechanistically informative systems: cytokinetic contractile rings, epithelial wound-edge purse strings, and adherens junction-associated actin belts. Across these contexts, ring assembly can be parsed into a series of conserved stages, including spatial confinement, membrane anchoring, actin nucleation and elongation, multivalent scaffolding, filament cross-linking and stabilization, regulated turnover, and force production. This comparative perspective uncovers shared design principles that may also apply to axons and offers a conceptual framework for dissecting the molecular basis of MPS nucleation, assembly, and long-term stability.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 8","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70534","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148617045","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":"Activation of GCaMP6f-Expressing Chromaffin and Satellite Glial Cells in Murine Adrenal Slices by Nanosecond Electric Pulses","authors":"Ciara Viola,&nbsp;Lisha Yang,&nbsp;Vasilii Mansurov,&nbsp;Jose Moreno Duran,&nbsp;Nicole M. Procacci,&nbsp;Jihwan Yoon,&nbsp;Normand Leblanc,&nbsp;Gale L. Craviso,&nbsp;Josette Zaklit,&nbsp;Thomas W. Gould","doi":"10.1111/jnc.70525","DOIUrl":"10.1111/jnc.70525","url":null,"abstract":"<div>\u0000 \u0000 <p>Nanosecond electric pulses (NEP) are being explored as a novel bioelectric stimulus to modulate neurosecretion. Recently we reported that NEP trigger transient, voltage-gated Ca²⁺ channel-mediated Ca²⁺ influx in cultured murine adrenal chromaffin cells (ACC) expressing the genetically-encoded Ca²⁺ indicator GCaMP6f. The present study investigated ACC Ca²⁺ responses to NEP in acute adrenal slices from mice that expressed GCaMP6f in both ACC and satellite glial cells (SGC), as well as exclusively in SGC. Adrenal glands from male and female mice were sectioned into 100 μm slices that were placed in a chamber and perfused at a rate of 3–4 mL/min with a balanced salt solution maintained at 35°C. A custom-fabricated non-contact electrode delivered NEP ranging from 12 to 90 ns to a large area of the adrenal medulla. Our results show that a single 30 ns pulse elicited a rapid, transient rise in intracellular Ca²⁺ in ACC in situ. Like NEP-induced Ca²⁺ responses in cultured ACC, ACC Ca²⁺ responses in situ depended on extracellular Ca²⁺ and voltage-gated Ca²⁺ channel activation. The nicotinic receptor antagonist hexamethonium failed to inhibit these responses, indicating that NEP stimulation, in contrast to stimulation with conventional duration electrical pulses, activates ACC directly rather than indirectly through activation of splanchnic nerve terminals. Furthermore, NEP exposure of the adrenal medulla also resulted in Ca²⁺ increases in surrounding SGC that were slower in onset and longer in duration than those evoked by NEP in ACC. Finally, comparison of Ca²⁺ responses elicited by NEP trains in ACC in situ to those evoked by such trains in ACC in vitro revealed that the native tissue environment promotes more highly synchronized Ca²⁺ responses. Together, these results lay the foundation for future studies exploring the potential for NEP to modulate catecholamine release from ACC remotely and non-invasively in vivo.</p>\u0000 <p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 7","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148549232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Novel Blood-Based Assay for Brain-Derived Tau and Its Validation in Traumatic Brain Injury","authors":"Wasiu G. Balogun,&nbsp;Xuemei Zeng,&nbsp;Michel N. Nafash,&nbsp;Anuradha Sehrawat,&nbsp;Ruyu Shi,&nbsp;Sarah E. Svirsky,&nbsp;David O. Okonkwo,&nbsp;Ava M. Puccio,&nbsp;Thomas K. Karikari","doi":"10.1111/jnc.70518","DOIUrl":"https://doi.org/10.1111/jnc.70518","url":null,"abstract":"<p>Brain-derived tau (BD-tau) is an emerging blood-based biomarker for neurodegeneration, yet there are currently limited well validated BD-tau assays available for research and clinical use. To enhance access to this vital biomarker for neurological disorders including traumatic brain injury (TBI), we developed a novel blood-based immunoassay for BD-tau on the ultra-sensitive Quanterix HD-X platform using Single Molecule Array technology. Analytical validation assessed dilution linearity, specificity, precision, detection limits, and spike recovery, each recording robust metrics in agreement with international expert recommendations. The assay demonstrated robust validation metrics, achieving between-run stability of 95% when analyzing aliquots from six independent plasma and serum samples across five analytical runs. It also showed strong dilution linearity when diluted four-fold and achieved over 90% recovery when spiked with cerebrospinal fluid. Next, we evaluated the clinical utility of the assay in cohorts of individuals with traumatic brain injury (TBI), where strong performances were recorded whether using the 2-step or 3-step assay formats (<i>ρ</i> = 0.94; <i>p</i> &lt; 0.0001). Furthermore, plasma BD-tau distinguished samples from TBI patients based on time from injury and severity (AUC = 0.93). Plasma BD-tau differentiated between favorable and unfavorable functional outcomes in the acute-severe group. Our findings underscore the significant potential of the BD-tau assay as a biomarker for TBI in the severe phase.</p><p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 7","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.70518","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467236","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":"Etv5 Is Required for Proper Maturation and Dendritic Development of Adult-Born Granule Cells in the Dentate Gyrus","authors":"Antonella S. Ríos,&nbsp;Solana F. López,&nbsp;Fernando Federicci,&nbsp;Paula A. Fontanet,&nbsp;Gustavo Paratcha,&nbsp;Fernanda Ledda","doi":"10.1111/jnc.70521","DOIUrl":"10.1111/jnc.70521","url":null,"abstract":"<div>\u0000 \u0000 <p>Adult neurogenesis in the dentate gyrus (DG) of the hippocampus is a dynamic and tightly regulated process that is finely regulated by a diverse array of transcription factors. While the transcription factor Etv5, a member of the Erythroblast Transformation Specific (ETS) family, has been implicated in embryonic development by regulating cell proliferation and differentiation across various tissues, its specific role in adult hippocampal neurogenesis remains unexplored. Here, we show that conditional ablation of <i>Etv5</i> specifically in adult-born granule cells (GCs) increases the proportion of Doublecortin (DCX)-positive immature GCs at the expense of mature neurons, without affecting the proportion of neither radial glia-like cells (RGCs) nor SOX2⁺ progenitor cells within the neurogenic niche. Furthermore, <i>Etv5</i> conditional mutant mice exhibit reduced dendritic complexity and defects in spine development, indicating impaired neuronal maturation and suggesting deficits in synaptic integration of adult-born GC neurons.</p>\u0000 <p>\u0000 \u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>\u0000 </div>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":"170 7","pages":""},"PeriodicalIF":4.6,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}