Journal of Neuroscience Research最新文献

{"title":"An Examination of Task-Evoked fMRI Data Processing in Functional Connectivity","authors":"Alice Giubergia,&nbsp;Sara Mascheretti,&nbsp;Valentina Lampis,&nbsp;Tommaso Ciceri,&nbsp;Martina Villa,&nbsp;Chiara Andreola,&nbsp;Filippo Arrigoni,&nbsp;Alessandra Bertoldo,&nbsp;Denis Peruzzo","doi":"10.1002/jnr.70132","DOIUrl":"10.1002/jnr.70132","url":null,"abstract":"<p>Although functional connectomics typically relies on resting-state fMRI, its analytical methods have been applied to task fMRI data in the investigation of broader involvements of brain regions even if inactive during a specific task. The purpose of this study is to assess the feasibility of inferring a true resting-state connectivity from task-fMRI data and to investigate the impact of connectomic-based analysis on behavioral trait studies. To this purpose, subjects underwent two visual fMRI tasks. The Blood-Oxygen-Level-Dependent (BOLD) time-series were processed to get both a “task” condition and a “pseudo-resting” condition applying different task regression setups to derive connectomes. Stimulus-classification experiments were conducted to compare “task” and “pseudo-resting” connectomes. Additionally, the influence of task regression was assessed through a classification experiment comparing children with Developmental Dyslexia (DD) and Typical Readers (TR). While task regression successfully removes task-related content from fMRI signals, stimulus information could still be inferred from connectomes, regardless of the preprocessing method used. Furthermore, a Support Vector Machine (SVM) experiment effectively discriminates between DD and TR in both “task” and “pseudo-resting” conditions. The study explored the impact of preprocessing in task fMRI experiments analyzed with connectomics. The ability to classify the stimuli in “pseudo-resting” conditions suggests that connectomes retain task-related signals even after task regression. Discriminative connections vary across tasks, affecting how classifiers differentiate between DD and TR. Despite these task-related differences, preprocessing had no effect on the inference of classification rules, indicating that key features are similarly evaluated in both tasks.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210763","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":"Association of Interhemispheric Structural Integrity With Transcallosal Interhemispheric Inhibition in People With Chronic Stroke","authors":"Brice Thomas Cleland,&nbsp;Amanda Bardhoshi,&nbsp;Sangeetha Madhavan","doi":"10.1002/jnr.70143","DOIUrl":"10.1002/jnr.70143","url":null,"abstract":"<div>\u0000 \u0000 <p>After stroke, interhemispheric communication is often disrupted. Interhemispheric inhibition after transcranial magnetic stimulation (TMS) is thought to be mediated through the corpus callosum, but no studies have directly tested this association in people with chronic stroke. This study determined the association between TMS interhemispheric inhibition and structural integrity of the pathway connecting the bilateral motor cortices through the corpus callosum in people with chronic stroke. 33 individuals with chronic stroke [60.7 (8.3) years old; 24 male; 8.6 (6.6) years post-stroke] were enrolled. From a diffusion-weighted scan, fractional anisotropy (FA) values were extracted from the pathway between the lower limb representations of the motor cortices via the corpus callosum. TMS interhemispheric inhibition was assessed as the ipsilateral silent period (iSP) in both legs. We tested associations between FA of the corpus callosum, TMS iSP, motor impairment [Fugl Meyer Lower Extremity Assessment (FMLE)], and interlimb coordination. Fractional anisotropy values (mean [SD]: 0.35 [0.07]) were indicative of white matter damage in the corpus callosum. Ipsilateral silent periods were identified in the non-paretic (<i>n</i> = 31, mean [SD]: 59.9 [41.3]) and paretic TA (<i>n</i> = 24, mean [SD]: 60.8 [22.2]). Larger FA values were associated with shorter iSP duration in the paretic TA (<i>R</i>² = 0.24, <i>p</i> = 0.02), better interlimb coordination (<i>R</i>² = 0.19, <i>p</i> = 0.02), and lesser motor impairment (<i>R</i>² = 0.14, <i>p</i> &lt; 0.05). Results suggest that TMS interhemispheric inhibition is at least partially mediated via the corpus callosum. Preservation of corpus callosum after stroke may allow interhemispheric inhibition and motor function and coordination that more closely resembles that of individuals without stroke.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199418","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":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148096786","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":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148096785","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":"Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude","authors":"Hongqiao Chen,&nbsp;Mingli Chen,&nbsp;Lian Meng,&nbsp;Xing Wei,&nbsp;Yan Qin,&nbsp;Zhumei Bi","doi":"10.1002/jnr.70130","DOIUrl":"10.1002/jnr.70130","url":null,"abstract":"<p>Ischemic stroke (IS) remains a devastating condition with limited neuroprotective options. This study investigated the role of the transcription factor inhibitor of DNA binding 3 (ID3) in acute IS through an integrated approach. Combining bioinformatic analysis of Gene Expression Omnibus (GEO) datasets with machine learning (ML) algorithms, we identified ID3 as a consistently downregulated key gene, and its expression level correlated with neurological severity. Functional analysis suggested ID3 modulates neuroinflammation. Furthermore, ID3 and C-type lectin domain family 4 member E (CLEC4E) showed potential as diagnostic biomarkers. Using network pharmacology, pantothenic acid (PA) was predicted as a potential ID3-targeting drug. This was preliminarily tested in an oxygen–glucose deprivation/reperfusion (OGD/R) model, where PA treatment specifically upregulated ID3, ameliorated neuronal electrophysiological dysfunction, and restored action potential amplitude. Our work provides the first integrative evidence suggesting ID3 as a pivotal protective factor in acute IS and nominates PA as a candidate for further development as a neuroprotective agent.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13172942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147930535","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":"Angiotensin-II Type 1 and Type 2 Receptors Differentially Regulate TWIK1 Potassium Channel Expression in Wistar Rat Sensory Neurons","authors":"Emanuel David Peralta,&nbsp;Sergio Gonzalo Benitez,&nbsp;Yanaysis Stable García,&nbsp;Cristian Gabriel Acosta","doi":"10.1002/jnr.70127","DOIUrl":"10.1002/jnr.70127","url":null,"abstract":"<div>\u0000 \u0000 <p>Two-pore domain potassium (K2P) channels control resting membrane potential of neurons and contribute to pain hypersensitivity when their expression or function is reduced. Tandem of P-domains in a Weak Inwardly rectifying K⁺ channel 1 (TWIK1) is broadly expressed in the nervous system, yet little is known about its regulation in dorsal root ganglion (DRG) neurons. Because components of the renin–angiotensin system (RAS) modulate sensory excitability, we investigated whether Angiotensin-II (Ang II) and its receptors, AT1R and AT2R, regulate TWIK1 expression. Using primary DRG cultures, we found that Ang II significantly increased TWIK1 mRNA and protein at 1–2 days in vitro. Quantitative immunocytochemistry revealed receptor-specific effects: TWIK1 up-regulation at 1 day was primarily AT2R-dependent, whereas AT1R contributed to a lesser extent. TWIK1 expression declined by 2 days but remained sensitive to receptor blockade. To test physiological relevance, we injected Ang II intradermally into the hindpaw of adult rats. Repeated—but not single—Ang II injections produced a modest reduction of TWIK1 in large L5 DRG neurons and in NF200-positive cutaneous terminals. This decrease was accompanied by mild mechanical hypersensitivity without changes in cold sensitivity. These in vivo effects align with preferential AT1R expression in medium and large DRG neurons and with the in vitro finding that TWIK1 down-regulation is most evident when AT1R remains active. These results identify TWIK1 as a downstream target of Ang II signaling in sensory neurons and suggest that RAS-dependent modulation of K2P channels may influence neuronal excitability and contribute to pain-related processes.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645664","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":"Correction to “Zinc Deficiency and Supplementation in Autism Spectrum Disorder and Phelan-McDermid Syndrome”","authors":"","doi":"10.1002/jnr.70128","DOIUrl":"10.1002/jnr.70128","url":null,"abstract":"<p>Alsufiani, H. M., A. S. Alkhanbashi, N. A. Bin Laswad, et al. 2022. “Zinc Deficiency and Supplementation in Autism Spectrum Disorder and Phelan-McDermid Syndrome.” <i>Journal of Neuroscience Research</i> 100, no. 4: 970–978. https://doi.org/10.1002/jnr.25019.</p><p>In the original published article, an error was identified in the reported prevalence of autism spectrum disorder (ASD).</p><p>In both the <b>Abstract</b> (“Approximately 1 in 36 children are diagnosed with autism spectrum disorder (ASD)”) and the <b>first paragraph of the Introduction</b> (“Around one in 36 children are diagnosed with autism, and it is four times more common in males than in females”), the prevalence was incorrectly stated as <b>1 in 36</b>.</p><p>The correct prevalence, based on the cited data, is <b>1 in 59</b>.</p><p>We apologize for this error.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627938","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 Transcription Factors Six3 and Six6 in Neuromedin-S Neurons Differentially Affect Circadian Rhythms","authors":"Brooke M. Van Loh,&nbsp;Geneva A. Dunn,&nbsp;Lauren E. Chun,&nbsp;Meera M. Patel,&nbsp;Nay Chi P. Naing,&nbsp;Duong Nguyen,&nbsp;Alexandra M. Yaw,&nbsp;Michael R. Gorman,&nbsp;Jessica Cassin,&nbsp;Pamela L. Mellon,&nbsp;Hanne M. Hoffmann,&nbsp;Karen J. Tonsfeldt","doi":"10.1002/jnr.70123","DOIUrl":"10.1002/jnr.70123","url":null,"abstract":"<p>Circadian rhythms are ~24-h rhythms generated by the suprachiasmatic nucleus (SCN) in the mammalian hypothalamus. The regulation of circadian rhythms and downstream processes is highly dependent on the proper development and function of the SCN. <i>Six3</i> and <i>Six6</i> are homologous homeodomain transcription factors that have been shown to be required for SCN development; intriguingly, both <i>Six3</i> and <i>Six6</i> remain expressed in the adult SCN. To determine the role of <i>Six3</i> and <i>Six6</i> in the SCN after neurogenesis, we used Cre-lox to conditionally knockdown either <i>Six3</i> or <i>Six6</i> from cells that express neuromedin-S (NMS), a neuropeptide expressed in approximately half of SCN neurons. We found that the <i>Nms</i>^<i>cre</i> allele turns on in the SCN after embryonic Day 16.5, limiting Cre-lox-mediated loss of <i>Six3</i> or <i>Six6</i> to the period after SCN neurogenesis. Using this approach, we hypothesized that <i>Six3</i> and <i>Six6</i> in NMS neurons regulate SCN circadian output and resulting reproductive function in males and females. Loss of <i>Six6</i> from NMS neurons had no impact on puberty and reproduction. While loss of <i>Six3</i> from NMS neurons had no effect in females, we found significantly decreased sperm motility in males, potentially through direct effects of <i>Six3</i> in the testis. Loss of <i>Six3,</i> but not <i>Six6</i>, in NMS neurons resulted in shortened wheel-running periods in constant darkness, indicating a shortening of the endogenous rhythm within the SCN. Together, these data indicate a role of <i>Six3</i> in determining the circadian period, suggesting differing functions of <i>Six3</i> and <i>Six6</i> in the adult SCN.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147623180","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":"Acute Opioid Receptor Blockade Restores Vascular Endothelial Growth Factor and Astrocyte Response in db/db Mouse Brain Following Hypoxia-Ischemic Injury","authors":"Rashmi Kumari,&nbsp;Elizabeth A. Proctor,&nbsp;Patricia McLaughlin","doi":"10.1002/jnr.70125","DOIUrl":"10.1002/jnr.70125","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetes plays an important role in the pathogenesis of ischemic stroke and brain recovery. We have reported the neuroprotective effect of low dose naltrexone (LDN) in type 2 diabetic (<i>db/db)</i> mice post-hypoxia-ischemia (HI) injury. In this study, we explored LDN mediated mechanisms of neuroprotection in diabetic mice. Adult male <i>db/db</i> and non-diabetic (<i>db/+)</i> mice underwent right common carotid artery occlusion followed by hypoxia (8% O₂) for 20 min. LDN (1 mg/kg) was administered at 4, 24, and 48 h post-HI, and mice were euthanized at 72 h. Blood and brain tissue were analyzed for cytokines and growth factors by multiplex array, immunofluorescence and western blotting. LDN treatment resulted in an increased number of reactive astrocytes in the motor cortex and caudate and hippocampus of diabetic mice, which was decreased in <i>db/+</i> mice, except in the CA3 hippocampal region. LDN did not show any significant change in the cytokine response between <i>db/+</i> and <i>db/db</i> mice. However, the vascular endothelial growth factor (VEGF) levels in the plasma and brain tissue of LDN-treated <i>db/db</i> mice that were significantly reduced in the vehicle-treated <i>db/db</i> group were restored to the level of the <i>db/+</i> treated group. When infarct size was categorized, LDN increased VEGF+ neurons in the motor cortex and caudate in small infarcts, and in the motor cortex of large infarcts, in <i>db/db</i> mice. The study suggests that acute LDN increased the number of VEGF+ neurons and prevented astrocytic cell death in <i>db/db</i> mice, thus enhancing neuroprotection following brain HI injury.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 4","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147609233","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":"Age and Maturation Stage Linked Consequences of Fibrinogen on Human Oligodendroglia","authors":"Gabriela J. Blaszczyk,&nbsp;Chao Weng,&nbsp;Abdulshakour Mohammadnia,&nbsp;Qiao-Ling Cui,&nbsp;Arianna Giurleo,&nbsp;Adam M. R. Groh,&nbsp;Chloe Plouffe,&nbsp;Julien Sirois,&nbsp;Valerio E. C. Piscopo,&nbsp;Moein Yaqubi,&nbsp;Asad Taqvi,&nbsp;Erin Cassidy,&nbsp;Liam Callahan Martin,&nbsp;Jeffery A. Hall,&nbsp;Roy W. R. Dudley,&nbsp;Myriam Srour,&nbsp;Stephanie E. J. Zandee,&nbsp;Wendy Klement,&nbsp;Sandra Larouche,&nbsp;Alexandre Prat,&nbsp;Thomas M. Durcan,&nbsp;Jo Anne Stratton,&nbsp;Jack P. Antel,&nbsp;G. R. Wayne Moore","doi":"10.1002/jnr.70120","DOIUrl":"10.1002/jnr.70120","url":null,"abstract":"<p>Fibrinogen is a blood-derived protein involved in coagulation and can make its way into the central nervous system (CNS) following breakdown of the blood–brain barrier. This molecule has been implicated in multiple sclerosis (MS), a disease marked by inflammation and demyelination in the CNS. However, the effect of this molecule has not been studied on human myelinating cells. This study examines how fibrinogen influences human oligodendrocyte (OL) lineage cells at various stages of development. Using induced pluripotent stem cell-derived (iPSC) OL precursors and human primary OLs, we examined the effects of fibrinogen on cell differentiation, viability, and myelination-related function. Here we show the differential effect of fibrinogen, based on OL-lineage stage. While fibrinogen induced aberrant differentiation of early lineage OLs, by inhibiting their maturation and inducing an astrocytic phenotype, on mature OLs fibrinogen was found to promote myelination capacity, as shown by ensheathment assays as well as on the RNA level. These effects were associated with the activation of bone morphogenetic protein (BMP) signaling, both in early and mature OLs. We further found BMP signaling enrichment in OLs to be correlated with the inflammatory activity of an MS lesion and confirmed fibrinogen deposition on OLs in situ. Unlike previous rodent studies, these findings indicate that fibrinogen has a lineage-dependent effect, where it may be inhibitory earlier in the lineage while promoting OL function in later stages. Understanding this dual role will provide insight into remyelination failure in MS and highlights the importance of timing and target in future therapeutic strategies.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"104 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13006721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499184","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}