Journal of integrative neuroscience最新文献

{"title":"Stimulator of Interferon Genes (STING)-Type I Interferon Signaling: Bridging Immunity and Pain.","authors":"Ti-Chuan Chiu, Yu-Yu Li, Chia-Hung Yu, Kuo-Chuan Hung, Chin-Chen Chu, Ping-Hsun Feng, Ping-Heng Tan","doi":"10.31083/JIN33414","DOIUrl":"https://doi.org/10.31083/JIN33414","url":null,"abstract":"<p><p>Interferons (IFNs) are cytokines with diverse functions, possessing antiviral, antiproliferative, and immunomodulatory effects. IFN-α and IFN-β, key members of the type I interferon (IFN-I) family, are widely used in the treatment of diseases such as hepatitis and multiple sclerosis. In the nervous system, microglia, astrocytes, and neurons express IFN-I receptors. Beyond their classical transcriptional roles, IFN-Is can suppress neuronal activity and synaptic transmission through nongenomic mechanisms, producing potent analgesic effects. However, IFN-Is are active in signaling pathways such as phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinase (MAPK), and the MAPK-interacting serine/threonine-protein kinase (MNK)-eukaryotic initiation factor 4E (eIF4E) pathway, which can sensitize peripheral nociceptors and contribute to nociceptive responses. This narrative review explores recent advances in understanding the roles of IFN-I and the cyclic-GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling cascade in acute and chronic nociceptive responses, which are increasingly recognized but remain a subject of debate. Recent studies suggest that the STING-IFN-I pathway has complex, stage-dependent effects on nociception. In the middle to late stages of the nociceptive response, this pathway can activate signal transducer and activator of transcription (STAT) signaling, as well as microglial mediated STING pathways and tumor necrosis factor (TNF) receptor-associated factor (TRAF) family member-associated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB activator) collectively referred to as TANK. These pathways increase pro- and anti-inflammatory cytokine production, promote microglial M1 polarization, and inhibit endoplasmic reticulum-phagy (ER-phagy) in the central nervous system (CNS). These mechanisms contribute to central sensitization while modulating the analgesic effects of IFN-Is. Thus, the STING-IFN-I pathway plays a dual role in nociception, with both pro-nociceptive and analgesic effects that are dependent on the stage of the nociceptive response. Understanding the differential roles of STING-IFN-I signaling in nociceptors under physiological and pathological conditions could pave the way for the development of targeted nociceptive response management therapies.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"33414"},"PeriodicalIF":2.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Genes for Improving Cold Sensitivity in Nerve-Damaged Rats Via Lumbar Sympathectomy Using Poly(A)-seq.","authors":"Xi Meng, Hanrui Fan, Ping Xu, Lei Yang, Yong Fei, Wenping Zhang","doi":"10.31083/JIN36253","DOIUrl":"https://doi.org/10.31083/JIN36253","url":null,"abstract":"<p><strong>Background: </strong>Lumbar sympathectomy improves blood flow to the lower limbs and is widely used in clinical practice to treat lower limb pain and cold. However, the therapeutic mechanisms underlying lumbar sympathectomy for limb coldness resulting from nerve injury remain unclear. This study aimed to investigate the effect of lumbar sympathectomy on cold allodynia in rats with spared nerve injury (SNI) and identify potential target genes associated with its analgesic effects.</p><p><strong>Methods: </strong>A rat model of SNI was established. Mechanical and cold pain thresholds were assessed in rats with SNI to explore the analgesic effects of lumbar sympathetic neurectomy on cold allodynia. Poly(A)-seq was used to analyze the transcriptional profile of the spinal cord. Differentially expressed genes (DEGs) were screened and analyzed using bioinformatics and validated by quantitative PCR analysis.</p><p><strong>Results: </strong>Lumbar sympathectomy improved mechanical pain, cold allodynia, and cold sensitivity in the ipsilateral hind paw of SNI rats (all <i>p</i> < 0.05). Poly(A)-seq identified 278 DEGs (177 upregulated and 101 downregulated) in the spinal cords of SNI model rats compared with control rats. We identified 174 DEGs in the gene expression profile of lumbar sympathectomized SNI rats, including 69 upregulated and 105 downregulated genes, compared with SNI model rats. Functional analysis of the DEGs revealed that the most significantly enriched pathways included immune-related pathways and cellular molecular components, which mediate neuroinflammation, central sensitization, and chronic pain. To explore the correlation among the DEGs, we used the STRING database to construct protein-protein interaction networks. Finally, quantitative PCR analysis revealed six potential target genes associated with cold analgesic effects epithelial mitogen gene (<i>EPGN</i>), histone cluster 2 H3 family member C2 (<i>Hist2h3c2</i>), small integral membrane protein 6 (<i>Smim6</i>), family with sequence similarity 187 member a (<i>FAM187A</i>), <i>LOC108349650</i>, and <i>LOC102550818</i>.</p><p><strong>Conclusions: </strong>Lumbar sympathectomy may alleviate cold allodynia in SNI model rats. We identified key genes associated with pain mitigation, offering potential therapeutic targets. These genes may serve as targets for treating nerve injury-induced cold allodynia. These findings provide valuable insights for the development of new treatments for nerve-related pain disorders.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"36253"},"PeriodicalIF":2.5,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EEG-Based Classification of Parkinson's Disease With Freezing of Gait Using Midfrontal Beta Oscillations.","authors":"Shotabdi Roy, Joseph Nuamah, Taylor J Bosch, Richa Barsainya, Maximilian Scherer, Thomas Koeglsperger, K C Santosh, Arun Singh","doi":"10.31083/JIN39023","DOIUrl":"https://doi.org/10.31083/JIN39023","url":null,"abstract":"<p><strong>Background: </strong>Freezing of gait (FOG) is a debilitating motor symptom of Parkinson's disease (PD) that significantly affects patient mobility and quality of life. Identifying reliable biomarkers to distinguish between PD patients with freezing of gait (PDFOG+) and those without FOG (PDFOG-) is essential for early intervention and treatment planning. This study investigates the potential of electroencephalographic (EEG) signals, focusing on well-studied midfrontal beta oscillatory feature, to classify PDFOG+ and PDFOG- using machine learning (ML) and deep learning (DL) approaches.</p><p><strong>Methods: </strong>Resting-state EEG data were collected from the midfrontal 'Cz' and nearby channels (Cz-cluster) from 41 PDFOG+ and 41 PDFOG- subjects. A range of ML and DL models, including logistic regression (LR), random forest (RF), extreme gradient boosting (XGBoost), categorical boosting (CatBoost), and long short-term memory (LSTM) models were evaluated using leave-one-subject-out (LOSO), 10-fold, and stratified cross-validation (CV).</p><p><strong>Results: </strong>Outcomes demonstrate that while LR achieved an area under the receiver-operating characteristic (AUC-ROC) score of 0.63, LSTM outperformed all models, achieving an AUC-ROC of 0.68 and accuracy of 0.63, particularly with the Cz-cluster configuration.</p><p><strong>Conclusions: </strong>These findings support the potential of midfrontal beta oscillations, particularly in combination with LSTM temporal modeling, a promising EEG-based biomarker for distinguishing PDFOG+ from PDFOG-. This work contributes to the development of more effective diagnostic tools and treatment strategies for PD-related gait impairments.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"39023"},"PeriodicalIF":2.5,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Muscone Protects Against Ferroptosis-Induced Injury in Models of Acute Ischemic Stroke by Modulating Snap25 Protein.","authors":"Ruijia You, Bin Sun, Jing Luo, Guanhua Hu, Nan Shao, Wenwen Si","doi":"10.31083/JIN39116","DOIUrl":"https://doi.org/10.31083/JIN39116","url":null,"abstract":"<p><strong>Background: </strong>Acute ischemic stroke (AIS) is one of the leading critical neurological conditions globally, resulting in significant adult mortality and disability. Previous studies have demonstrated a close relationship between AIS and the ferroptosis signaling pathway. Muscone, the primary active small-molecule component of musk, is a traditional Chinese medicine that exhibits significant pharmacological effects in reducing stroke injury. However, there is still only limited research on whether muscone can modulate ferroptosis-related injury in AIS, and on the underlying regulatory molecular mechanisms.</p><p><strong>Methods: </strong>We utilized a transmission electron microscope and concurrently performed assays for glutathione peroxidase 4 (GPX4) activity, glutathione (GSH), reactive oxygen species (ROS), lipid peroxides, as well as cell viability and live/dead cell staining to investigate alterations in ferroptosis levels. RNA sequencing, bioinformatics analysis, and western blot (WB) assays were employed to evaluate the changes in synaptosome-associated protein 25 kDa (Snap25) expression levels. Furthermore, molecular docking, surface plasmon resonance (SPR) detection, and molecular dynamics (MD) simulation were implemented to examine the binding affinity and interaction between muscone and Snap25.</p><p><strong>Results: </strong>RNA sequencing technology, bioinformatics analysis, and WB assays revealed that Snap25 was specifically downregulated under simulated AIS conditions. Snap25 knockdown and overexpression experiments were also conducted to elucidate the molecular mechanism by which muscone modulates Snap25 expression, thereby mitigating ferroptosis injury in AIS. Additionally, the results of molecular docking, SPR detection, and MD simulations indicate that muscone has multiple binding sites that allow it to bind directly to the Snap25 protein, thereby stabilizing the protein structure.</p><p><strong>Conclusions: </strong>Our findings suggest that muscone produces an anti-AIS effect in the context of AIS injury by increasing Snap25 protein expression, thus reducing ferroptosis. This investigation offers insight into the anti-stroke mechanism of muscone and introduces a promising new treatment option for clinical AIS management.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"39116"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Idebenone Orchestrates Anti-Inflammatory and Antioxidant Responses to Alleviate Brain Injury After Intracerebral Hemorrhage in Mice.","authors":"Chen Chen, Liang Cao, Mengzhou Xue, Ning Zhu","doi":"10.31083/JIN37182","DOIUrl":"https://doi.org/10.31083/JIN37182","url":null,"abstract":"<p><strong>Background: </strong>Intracerebral hemorrhage (ICH) is a critical form of stroke with limited treatment options, with secondary brain injury significantly affecting patient outcomes. This study investigated the neuroprotective benefits of idebenone (IDE) in ICH.</p><p><strong>Methods: </strong>An ICH model was established in mice and the temporal progression of oxidative stress and neuroinflammation was evaluated. IDE was then administered intraperitoneally for 3 consecutive days to evaluate its therapeutic effects. Tissue histology was examined after staining with hematoxylin-eosin and TdT-mediated dUTP nick end labeling (TUNEL), while oxidative stress was assessed by western blotting and measurement of malondialdehyde (MDA) levels and neuroinflammation was examined using immunostaining, western blotting, and enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>Oxidative stress and neuroinflammation peaked at 3 days post-ICH, with elevated levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and significant microglial activation. IDE-treated mice had reduced hematoma volumes and improved neurological outcomes. IDE administration decreased Kelch-like ECH-associated protein 1 (Keap1) expression while increasing Nrf2 and NAD(P)H quinone oxidoreductase 1 (NQO1) levels, leading to reduced oxidative damage (<i>p</i> < 0.01, <i>p</i> < 0.05, and <i>p</i> < 0.05, respectively). Moreover, IDE attenuated microglial activation and neutrophil recruitment (<i>p</i> < 0.01, <i>p</i> < 0.01), reduced the levels of matrix metalloproteinase-9 (MMP-9), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) levels (<i>p</i> < 0.05, <i>p</i> < 0.05, and <i>p</i> < 0.05, respectively), and increased IL-10 expression (<i>p</i> < 0.01). IDE also preserved the integrity of the blood-brain barrier (BBB) and reduced brain edema.</p><p><strong>Conclusions: </strong>The results demonstrated that IDE exerts neuroprotective effects in ICH through the mitigation of oxidative stress and neuroinflammation during the acute injury phase. IDE may be a viable therapeutic intervention for ICH.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"37182"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Does Transcranial Direct Current Stimulation Improve Gait Performances in Healthy Older Adults? A Meta-Analysis.","authors":"Beom Jin Choi, Hajun Lee, Nyeonju Kang","doi":"10.31083/JIN36636","DOIUrl":"10.31083/JIN36636","url":null,"abstract":"<p><strong>Background: </strong>Aging can cause degenerative changes in motor and cognition-related brain areas, presumably by interfering with gait performance in healthy aging populations. We aimed to assess the effects of transcranial direct current stimulation (tDCS) on single- and dual-task walking performances in healthy older adults using meta-analytic approaches.</p><p><strong>Methods: </strong>Eleven studies were qualified based on the inclusion criteria: (a) healthy older adults, (b) treatment = tDCS protocols, (c) control = sham stimulation, (d) gait performance outcomes, and (e) randomized controlled trials using parallel or crossover designs. Effect sizes were estimated using standardized mean difference (SMD) to examine gait performances between active tDCS and sham stimulation. A separate random-effect meta-analysis was performed to determine the effects of tDCS protocols on gait performance during single- and dual-task walking tasks.</p><p><strong>Results: </strong>During single-task walking, the random-effects meta-analysis showed improvements in stride time variability (<i>SMD</i> = 0.203; <i>p</i> = 0.005) and functional mobility (<i>SMD</i> = 0.595; <i>p</i> < 0.001). Moreover, single-task walking performances were improved when the tDCS protocols targeted the primary motor cortex (<i>SMD</i> = 0.424; <i>p</i> = 0.005) and used off-line stimulation (<i>SMD</i> = 0.168; <i>p</i> = 0.008). During dual-task walking, tDCS improved gait speed (<i>SMD</i> = 0.177; <i>p</i> = 0.025) and dual-task cost for gait speed (<i>SMD</i> = 0.548; <i>p</i> < 0.001). Dual-task walking performances were advanced when the tDCS protocols targeted the dorsolateral prefrontal cortex (<i>SMD</i> = 0.231; <i>p</i> = 0.029) and multiple areas including prefrontal cortex (<i>SMD</i> = 0.382; <i>p</i> = 0.001), and applied off-line stimulation (<i>SMD</i> = 0.249; <i>p</i> < 0.001).</p><p><strong>Conclusions: </strong>These findings indicate that the tDCS protocols may be a promising tool to support mobility and reduce gait-related challenges in the healthy aging population.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"36636"},"PeriodicalIF":2.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impairment of White Matter Microstructure in Alcohol Use Disorders and Its Association With Symptoms.","authors":"Shuqi He, Qinghui Zhang, Li Wan, Yang Liu","doi":"10.31083/JIN37538","DOIUrl":"https://doi.org/10.31083/JIN37538","url":null,"abstract":"<p><strong>Background: </strong>Alcohol use disorder (AUD) is a global health concern, with alcohol abuse leading to structural damage to white matter (WM) fiber tracts, which are crucial for cognitive and emotional functions. However, existing studies often lack systematic evaluations of these changes and their clinical correlations.</p><p><strong>Methods: </strong>Using tract-based spatial statistics (TBSS), we analyzed diffusion tensor imaging (DTI) data from 20 AUD patients and 20 healthy controls. Correlations between fractional anisotropy (FA) values and clinical symptoms, including cognitive dysfunction, depression, and impulsivity, were examined.</p><p><strong>Results: </strong>AUD patients presented significantly decreased FA values in the right corpus callosum, right fornix, left inferior fronto-occipital fasciculus, and left cerebral white matter. The FA peak values of the right fornix and the left cerebral white matter were positively and significantly correlated with cognitive function scores in the AUD group after controlling for smoking status, age, and years of education.</p><p><strong>Conclusions: </strong>Alcohol abuse significantly impairs WM integrity, particularly in regions related to cognitive and emotional regulation. These findings provide structural evidence for the neurobiological mechanisms of AUD and suggest that FA may serve as a potential biomarker for assessing brain damage, guiding therapeutic interventions.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"37538"},"PeriodicalIF":2.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Motor Imagery Combined With Action Observation on Motor Function in Stroke Patients.","authors":"Aisha Nakintu, Carmelo Mario Vicario, Lijuan Wang, Shuo Luan, Fengxue Qi","doi":"10.31083/JIN26495","DOIUrl":"https://doi.org/10.31083/JIN26495","url":null,"abstract":"<p><p>Stroke symptoms encompass sensory, cognitive, motor, and psychosocial dysfunctions, with motor impairment being the most prevalent. This impairment significantly contributes to functional incapacity and a diminished quality of life. Stroke rehabilitation strategies primarily aim to promote neural reorganization and motor skill recovery. Among these, motor imagery (MI) and action observation (AO) are distinct therapeutic techniques with unique mechanisms of action. This review begins by analyzing the strengths and limitations of each approach individually and argues that integrating MI and AO therapy could offer a more effective rehabilitation strategy. A thorough evaluation of relevant literature is presented, detailing methodologies, key findings, and implications. The objective is to elucidate the potential benefits and underlying mechanisms of combining these two therapies in stroke rehabilitation. In conclusion, the article advocates for the adoption of combined MI and AO therapy in neurorehabilitation.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"26495"},"PeriodicalIF":2.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise Leads to Brain Glucose Metabolism Activation, Increased Dopamine D1 Receptor Levels and is Negatively Correlated with Social Behavior.","authors":"Michael Bobick, Colin Hanna, John Tyler, Patrick Mohr, Huy Lu, Aidan Powell, Kenneth Blum, David Baron, Kai-Uwe Lewandrowski, Igor Elman, Albert Pinhasov, Mark S Gold, Panayotis K Thanos","doi":"10.31083/JIN36646","DOIUrl":"https://doi.org/10.31083/JIN36646","url":null,"abstract":"<p><strong>Background: </strong>Exercise enhances overall health, playing an important role in protecting against diseases that impact brain function. Studies show that physical activity influences several key biological processes, including dopamine signaling, brain glucose metabolism (BGluM), and social behavior.</p><p><strong>Methods: </strong>Male sedentary and chronic exercise rats were examined for dopamine signaling and social behavior. Tyrosine hydroxylase (TH) immunohistochemistry (IHC), and D1 and D2 receptor (D1R and D2R) autoradiography was used to assess dopamine signaling; [18F]-Fluorodeoxyglucose positron emission tomography (FDG PET) was used to measure brain functional connectivity; Crawley's three-chamber sociability test was used to measure social behavior; and Pearson correlation was used to analyze correlations between social interaction and TH, D1R, and D2R binding.</p><p><strong>Results: </strong>Exercised rats demonstrated greater D1R binding within several regions of the caudate putamen and nucleus accumbens. PET image analysis showed significantly higher BGluM in the exercised rats compared with the sedentary controls across several brain regions. These regions are associated with enhanced functional connectivity related to movement, olfaction, cardiovascular function, and predator awareness. Exercise had no significant effect on social interaction. Pearson correlation analysis revealed a significant negative relationship between social interaction and D1R binding.</p><p><strong>Conclusions: </strong>Chronic aerobic exercise did not significantly alter social interaction, TH, or D2R binding. D1R binding was enhanced in the exercise group compared with the sedentary group and was negatively correlated with social interaction. We speculate that approach behavior was attenuated by exercise due to social threat stimulation. Functional connectivity imaging data showed significant glucose metabolic activation within the cuneiform nucleus, which has been previously shown to be critical in defensive behavior. This may explain the lack of significant effect of exercise on approach or exploratory behavior. These findings support the potential of exercise in response to social behavior and the possible attenuation of social behavior towards a social threat or socially inappropriate behavior. Exercise can induce metabolic transience that may assist rats in detecting odors from larger predatory animals.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"36646"},"PeriodicalIF":2.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Emerging Role of Filamin A and <i>FLNA</i> Gene in Central Nervous System Functions: Insights into Neurodevelopment and Disease.","authors":"Nikita I Golushko, Anton D Shevlyakov, Daniil D Martynov, Longen Yang, Murilo S de Abreu, Allan V Kalueff","doi":"10.31083/JIN26489","DOIUrl":"https://doi.org/10.31083/JIN26489","url":null,"abstract":"<p><p>Filamin A (FLNA) is a key protein that binds actin filaments to transmembrane integrins and plays an important role in maintaining cell shape and signaling. In the brain, FLNA is emerging as a critical regulator of neurodevelopment, neuronal migration, actin organization, and neuromodulation. Mutations and/or aberrant expression of the <i>FLNA</i> gene are associated with various brain diseases, such as periventricular heterotopia, Ehlers-Danlos syndrome, and other disorders with impaired cognitive function and brain maldevelopment. Here, we discuss the critical role of FLNA in brain function; its interactions with receptors, integrins, and signaling molecules, as well as the implications of its activity for brain health and disease.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"24 6","pages":"26489"},"PeriodicalIF":2.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}