Journal of Neuroscience Research最新文献

{"title":"A Novel H2S Donor Alleviates Neuroinflammation and Seizures by Inhibiting the C3-C3aR Pathway","authors":"Yaru Yang,&nbsp;Xutao Wang,&nbsp;Tiantian Wang,&nbsp;Xiao Wang,&nbsp;Honghao Xu,&nbsp;Lian Liu,&nbsp;Shuisheng Lei,&nbsp;Xiao qin Zhu","doi":"10.1002/jnr.70041","DOIUrl":"https://doi.org/10.1002/jnr.70041","url":null,"abstract":"<div>\u0000 \u0000 <p>Both astrocytes and microglia are activated in the epileptic brain. There is an interaction between them through the complement 3 (C3)-C3a receptor (C3aR) pathway, which plays a detrimental role in seizures. Our self-developed novel H₂S donor has been found to have anti-seizure effects. However, its mechanism remains to be explored. In the present study, we showed that the novel H₂S donor can inhibit the activation of astrocytes and microglia and their interaction through C3-C3aR signaling, which contributed to alleviating microglial neuroinflammation and seizures. In LPS-treated astrocytes and pilocarpine-induced epileptic mice, the H₂S donor reduced C3 production in astrocytes and regulated the expression of inflammatory cytokines IL-1β and IL-10 in microglia. The H₂S donor also reduced the EEG amplitude of hippocampal epileptic waves and relieved seizures in epileptic mice. These effects of the H₂S donor can be reversed by intranasal C3 treatment and mimicked by a C3aR antagonist. These findings provide a novel mechanism underlying the anti-seizure effects of the H₂S donor. Therefore, the H₂S donor has the potential to be used as a candidate for antiepileptic drugs.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897054","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":"Tubulin Polymerization Promoting Proteins: Functional Diversity With Implications in Neurological Disorders","authors":"Paloma J. Diaz,&nbsp;Qian Shi,&nbsp;Priscilla Y. McNeish,&nbsp;Swati Banerjee","doi":"10.1002/jnr.70044","DOIUrl":"https://doi.org/10.1002/jnr.70044","url":null,"abstract":"<p><i>T</i>ubulin <i>P</i>olymerization <i>P</i>romoting <i>P</i>roteins (TPPPs) are highly conserved across species but remain poorly understood. There are three <i>TPPP</i> genes in humans, with only one homologous <i>TPPP</i> gene in invertebrates, such as <i>Drosophila</i> and <i>C. elegans</i>. The human TPPP (TPPP1/p25/p25α) is enriched in the brain and shares sequence similarities with the invertebrate TPPPs. TPPP/p25 associates with microtubules and plays a pivotal role in microtubule dynamics, bundling, and polymerization, thereby stabilizing the microtubular network. This is essential for cytoskeletal organization and proper functioning of neurons and glial cells, including axonal growth, regeneration, migration, trafficking, synapse formation, and myelination of axons. However, studies have also uncovered that besides its cytoplasmic/microtubular localization, TPPP/p25 is present in other subcellular compartments, including the mitochondria and nucleus, underscoring the presence of additional novel functions. At the molecular level, TPPP/p25 is predicted to exist as an intrinsically disordered protein and is implicated in neurological and neurodegenerative disorders, including Parkinson's and related disorders and Multiple Sclerosis. In this article, we provide a comprehensive overview of TPPP/p25, highlighting its evolutionary conservation, cellular and subcellular localization, established and emerging functions in the nervous system, interacting partners, potential clinical relevance to human neurological disorders, and conclude with unresolved questions and future areas of study.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits","authors":"Lacey B. Sell,&nbsp;Carson Zabel,&nbsp;Sabine Weller Grønborg,&nbsp;Qian Shi,&nbsp;Manzoor A. Bhat","doi":"10.1002/jnr.70040","DOIUrl":"https://doi.org/10.1002/jnr.70040","url":null,"abstract":"<div>\u0000 \u0000 <p><i>CNTNAP1</i> encodes the contactin-associated protein 1 (Cntnap1) which localizes to the paranodal region in all myelinated axons and is essential for axonal domain organization and the propagation of action potentials. To date, close to 45 reported human <i>CNTNAP1</i> variants have been identified that are associated with dysregulation and disorganization of the axonal domains, resulting in various forms of congenital hypomyelinating neuropathies in children. Currently, no treatments are available for neuropathies caused by <i>CNTNAP1</i> variants, highlighting the importance of fully characterizing these mutations and their impact on Cntnap1 functions. To understand the importance of a novel human <i>CNTNAP1</i> likely pathogenic variant that changes glycine at position 349 to valine in a child who also carries a <i>CNTNAP1</i> truncation and displayed severe neurological deficits, we used <i>CRISPR/Cas9</i> methodology and introduced a single nucleotide substitution in the mouse <i>Cntnap1</i> gene, resulting in glycine at 350 to valine (<i>Cntnap1</i>^<i>G350V</i>). Trans-allelic combination of <i>Cntnap1</i>^<i>G350V</i> with a <i>Cntnap1</i> null allele (<i>Cntnap1</i>^{<i>G350V/−</i>}) mimics human pathologies, recapitulating hypomyelination neuropathies <i>associated with CNTNAP1</i> mutations as well as loss of paranodal junctions and disorganization of axonal domains in myelinated axons. Expression of the wild type <i>Cntnap1</i> transgene in <i>Cntnap1</i>^{<i>G350V/−</i>} mice rescued the mutant phenotypes and restored all neurological deficits. Our studies demonstrate that GGT (glycine) to GTT (valine) change in human <i>CNTNAP1</i> creates a recessive loss of function allele and lays the foundation for potential gene therapy studies aimed at treating <i>CNTNAP1</i>-associated hypomyelinating neuropathies in children.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861880","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":"EXPRESSION OF CONCERN: Lithium Inhibits Aβ-Induced Stress in Endoplasmic Reticulum of Rabbit Hippocampus but Does Not Prevent Oxidative Damage and Tau Phosphorylation","authors":"","doi":"10.1002/jnr.70031","DOIUrl":"https://doi.org/10.1002/jnr.70031","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: O. Ghribi, M. M. Herman and J. Savory, “Lithium Inhibits Aβ-Induced Stress in Endoplasmic Reticulum of Rabbit Hippocampus but Does Not Prevent Oxidative Damage and Tau Phosphorylation,” <i>Journal of Neuroscience Research</i> 71, no. 6 (2003): 853–862, https://doi.org/10.1002/jnr.10511.</p><p>This Expression of Concern is for the above article, published online on 04 February 2003 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and Wiley Periodicals LLC. The Expression of Concern has been agreed due to overlap between images presented in Figures 5H and 5I. Due to the time that has elapsed, the original raw data of this manuscript is no longer available. Although the conclusions are not believed to be affected, the journal is issuing this expression of concern to alert readers.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857182","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: Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures","authors":"","doi":"10.1002/jnr.70037","DOIUrl":"https://doi.org/10.1002/jnr.70037","url":null,"abstract":"<p><b>RETRACTION:</b> A. Campisi, V. Bramanti, D. Caccamo, G. Li Volti, G. Cannavò, M. Currò, G. Raciti, F. Galvano, F. Amenta, A. Vanella, R. Ientile, R. Avola, “Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures,” <i>Journal of Neuroscience Research</i> 86, no. 6 (2008): 1297–1305, https://doi.org/10.1002/jnr.21579.</p><p>The above article, published online on 26 November 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley &amp; Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 1 and 8 were duplicated and manipulated, and that portions of Figure 8 were duplicated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857178","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: Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture","authors":"","doi":"10.1002/jnr.70036","DOIUrl":"https://doi.org/10.1002/jnr.70036","url":null,"abstract":"<p><b>RETRACTION:</b> V. Bramanti, S. Grasso, D. Tibullo, C. Giallongo, R. Pappa, MV Brundo, D. Tomassoni, M. Viola, F. Amenta, and R. Avola, “Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture,” <i>Journal of Neuroscience Research</i> 94, no. 1 (2016): 90-98, https://doi.org/10.1002/jnr.23678.</p><p>The above article, published online on 15 October 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley &amp; Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 2B and 3 were duplicated and manipulated, and that most of the images from Figure 2A were duplicated and manipulated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856966","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":"EXPRESSION OF CONCERN: Gene Expression Profile Activated by the Chemokine CCL5/RANTES in Human Neuronal Cells","authors":"","doi":"10.1002/jnr.70038","DOIUrl":"https://doi.org/10.1002/jnr.70038","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN:</b> A. Valerio, M. Ferrario, F.O. Martinez, M. Locati, V. Ghisi, L. Grazia Bresciani, A. Mantovani, P. Spano, “Gene Expression Profile Activated by the Chemokine CCL5/RANTES in Human Neuronal Cells,” <i>Journal of Neuroscience Research</i> 78, no. 3 (2004): 371-382, https://doi.org/10.1002/jnr.20250.</p><p>This Expression of Concern is for the above article, published online on 23 August 2004 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley &amp; Sons, Inc. Following publication, concerns were raised by a third party that the control actin bands had been duplicated within Figure 2. While the image manipulation does not seem to affect the conclusions of the paper, the journal has decided to issue an Expression of Concern to inform and alert readers. The authors have been notified of the Expression of Concern.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856965","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":"Sex and Strain Differences in Analgesic and Hyperlocomotor Effects of Morphine and μ-Opioid Receptor Expression in Mice","authors":"Damien C. Boorman,&nbsp;Simran K. Rehal,&nbsp;Maryam Fazili,&nbsp;Loren J. Martin","doi":"10.1002/jnr.70039","DOIUrl":"https://doi.org/10.1002/jnr.70039","url":null,"abstract":"<p>Sex and gender differences in the analgesic efficacy and side effects of opioids have been widely reported, but their underlying neurobiological mechanisms remain poorly understood. Preclinical animal models are essential tools for investigating these differences and providing insights into the neurobiology of opioid effects. Although studies in rats have revealed sex-specific effects of opioids, the sex-dependent behavioral profiles of opioids in mice, particularly across strains, remain largely unexplored. In this study, we characterized sex and strain differences in the antinociceptive and hyperlocomotor effects of morphine in the two most widely used mouse strains—CD1 and C57BL/6—and quantified regional expression of the μ-opioid receptor (MOR) in key brain and spinal cord regions. Both strains exhibited clear, dose-dependent antinociceptive and hyperlocomotor responses to morphine. While no significant sex or strain differences were observed in antinociceptive effects, C57BL/6 mice displayed significantly greater hyperlocomotor activity than CD1 mice. Western blot analyses revealed strain-specific MOR expression, with CD1 mice showing higher spinal cord and periaqueductal gray MOR levels, particularly in females, while C57BL/6 mice exhibited elevated MOR expression in the caudoputamen. Morphine treatment increased spinal MOR expression in CD1 mice but not C57BL/6, suggesting strain-dependent regulation of MOR. These findings highlight strain-specific behavioral and molecular responses to morphine, emphasizing the importance of strain and sex considerations in preclinical opioid research.</p>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143845853","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":"Quantitative MRI of the Spinal Cord and Brain in Chronic Traumatic Spinal Cord Injury: In Vivo Assessment of Structural Changes","authors":"Jing Li,&nbsp;Xiaojing Zhao,&nbsp;Yi Shan,&nbsp;Guixiang Shan,&nbsp;Peng-Hu Wei,&nbsp;Lin Liu,&nbsp;Changming Wang,&nbsp;Hang Wu,&nbsp;Weiqun Song,&nbsp;Yi Tang,&nbsp;Guo-Guang Zhao,&nbsp;Jie Lu","doi":"10.1002/jnr.70030","DOIUrl":"https://doi.org/10.1002/jnr.70030","url":null,"abstract":"<div>\u0000 \u0000 <p>The prolonged survival of traumatic spinal cord injury (TSCI) patients underscores the need to customize rehabilitative treatment plans according to patients' characteristics, aiming to restore motor function. We conducted a cross-sectional study of two groups with chronic TSCI (short-term group: 11 patients with an injury time of 1–2 years; long-term group: 10 patients with an injury time &gt; 2 years) and 16 controls. Quantitative MRI was used to evaluate structural changes in the upper spinal cord and brain. Compared to controls, both groups exhibited decreased fractional anisotropy (close relationship of the decreased) in the spinal cord, and the long-term group showed reduced spinal cord cross-sectional areas. The short-term group presented increased gray matter volumes (GMVs) in the paracentral lobule, postcentral gyrus, and supplementary motor area, indicating compensatory neural changes, whereas the long-term group exhibited decreased GMV in cerebellar lobule VI, suggesting weakening of the signal received by the cerebellum. Track-based spatial statistics revealed the close relationship of the decreased FA was with the increased radial diffusivity in the long-term group, indicating that demyelination mainly altered the white matter. Correlation analysis revealed that the increased GMV was negatively correlated with the sensorimotor score (<i>r</i> = −0.725, <i>p</i> = 0.018). Additionally, the GMV of cerebellar lobule VI was positively correlated with the sensorimotor score (<i>r</i> = 0.671, <i>p</i> = 0.024). In summary, quantitative MRI identifies structural changes in the brain and spinal cord of patients with chronic TSCI that vary with the time since injury and provide imaging evidence for the development of precise targeted therapies.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818660","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":"Cannabidiol-Rich Cannabis sativa L. Extract Alleviates LPS-Induced Neuroinflammation Behavioral Alterations, and Astrocytic Bioenergetic Impairment in Male Mice","authors":"Hind Ibork,&nbsp;Zakaria Ait Lhaj,&nbsp;Khadija Boualam,&nbsp;Sara El Idrissi,&nbsp;Ahmet B. Ortaakarsu,&nbsp;Lhoussain Hajji,&nbsp;Annabelle Manalo Morgan,&nbsp;Farid Khallouki,&nbsp;Khalid Taghzouti,&nbsp;Oualid Abboussi","doi":"10.1002/jnr.70035","DOIUrl":"https://doi.org/10.1002/jnr.70035","url":null,"abstract":"<div>\u0000 \u0000 <p>Neuroinflammation is a hallmark of various neurodegenerative disorders, yet effective treatments remain limited. This study investigates the neuroprotective potential of a cannabidiol (CBD)-Rich <i>Cannabis sativa</i> L. (CS) extract in a lipopolysaccharide (LPS)-induced neuroinflammation mouse model. The effects on anxiety-like behavior, cognitive function, and locomotor activity were assessed using behavioral tests (open field, elevated plus maze, novel object recognition, and Morris water maze). Antioxidant activity was measured by assaying glutathione (GSH) levels and lipid peroxidation by-products (TBARs). Anti-inflammatory properties were evaluated using quantitative reverse transcription polymerase chain reaction (QRt-PCR) for proinflammatory cytokines (IL-6 and TNF-α), glial fibrillary acidic protein (GFAP), and cannabinoid receptor 1 (CB1) mRNAs in the prefrontal cortex (PFC). Astrocytic bioenergetics were analyzed using extracellular flux assays. Additionally, computational inference with a deep learning approach was conducted to evaluate the synergistic interactions among CS phytocompounds on the CB1 receptors. Compared with synthetic CBD, the CS extract (20.0 mg/kg) demonstrated superior efficacy in mitigating LPS-induced anxiety-like behavior, cognitive deficits, and locomotor impairments. It also significantly mitigated oxidative stress (increased GSH, reduced TBARs) and suppressed proinflammatory cytokines and GFAP mRNAs, indicating potent anti-inflammatory properties. The extract modulated CB1 receptor expression and preserved metabolic homeostasis in cortical astrocytes, preventing their shift from glycolysis to oxidative phosphorylation under neuroinflammatory conditions. Computational modeling highlighted conformational changes in CB1 receptor residues induced by Delta-9-THC that enhanced CBD binding. These findings underscore the potential of CS extract as a therapeutic candidate for managing neuroinflammation and its associated neurodegenerative consequences, warranting further clinical exploration.</p>\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143793626","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}