Journal of integrative neuroscience最新文献

{"title":"Epilepsy: Born in NREM Sleep?","authors":"Peter Halász, Anna Szűcs","doi":"10.31083/j.jin2308146","DOIUrl":"https://doi.org/10.31083/j.jin2308146","url":null,"abstract":"","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"146"},"PeriodicalIF":2.5,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108148","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":"Recent Insights into Hippocampal Dysfunction and Neuroplasticity in Sleep Disorders: An Update from Preclinical Studies.","authors":"Poornima D E Weerasinghe-Mudiyanselage, Changjong Moon","doi":"10.31083/j.jin2308144","DOIUrl":"https://doi.org/10.31083/j.jin2308144","url":null,"abstract":"<p><p>Sleep disorders are prevalent neurological conditions linked to neurocognitive impairments. Understanding the neuroplasticity changes in the hippocampus, which plays a central role in regulating neurocognitive function, is crucial in the context of sleep disorders. However, research on neurodegenerative disorders and the influence of sleep disorders on hippocampal neuroplasticity remains largely unclear. Therefore, this review aims to highlight the latest advancements regarding hippocampal neuroplasticity and functional changes during sleep disorders, drawing insights from clinical and preclinical research involving sleep-deprived animal models. These articles were gathered through comprehensive literature searches across databases, including Google Scholar, PubMed, Web of Science, and Scopus. Maternal sleep deprivation has been observed to cause neurocognitive impairment in offspring, along with changes in protein expression levels associated with neuroplasticity. Similarly, sleep deprivation in adult mice has been shown to affect several cognitive functions and fear extinction without influencing the acquisition of fear conditioning. While mechanistic research on neurocognitive dysfunction induced by maternal and adult sleep deprivation is limited, it suggests the involvement of several signaling pathways, including neurotrophic factors, synaptic proteins, and inflammatory molecules, which are triggered by sleep deprivation. Further studies are needed to clarify the mechanistic pathways underlying hippocampal dysfunction and synaptic alterations associated with sleep disturbances.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"144"},"PeriodicalIF":2.5,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108156","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":"Fingolimod Alleviates Inflammation after Cerebral Ischemia via HMGB1/TLR4/NF-κB Signaling Pathway.","authors":"Yao Xing, Liyuan Zhong, Jun Guo, Cuifen Bao, Yumin Luo, Lianqiu Min","doi":"10.31083/j.jin2308142","DOIUrl":"10.31083/j.jin2308142","url":null,"abstract":"<p><strong>Background: </strong>Clinically, ischemic reperfusion injury is the main cause of stroke injury. This study aimed to assess the effectiveness of fingolimod in suppressing inflammation caused by ischemic brain injury and explore its pharmacological mechanisms.</p><p><strong>Methods: </strong>In total, 75 male Sprague-Dawley rats were randomly and equally assigned to five distinct groups: sham, middle cerebral artery occlusion/reperfusion (MCAO/R) surgery, fingolimod low-dose (F-L), fingolimod medium-dose (F-M), and fingolimod high-dose (F-H). Neurobehavioral tests, 2,3,5-triphenyltetrazolium chloride staining, and the brain tissue drying-wet method were conducted to evaluate neurological impairment, cerebral infarction size, and brain water content. Enzyme-linked immunosorbent assay was employed to quantify pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) protein levels. Western blotting and immunohistochemical staining were performed to assess high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), and nuclear factor kappa-B p65 (NF-κBp65) levels.</p><p><strong>Results: </strong>Rats in the F-L, F-M, and F-H groups exhibited lower Longa scores, reduced infarction volumes, and decreased brain edema than those in the MCAO/R group. Additionally, the F-L, F-M, and F-H groups exhibited lower serum levels of IL-1β, IL-6, and TNF-α than those of the MCAO/R group. Additionally, F-L, F-M, and F-H treatments resulted in decreased HMGB1, TLR4, and NF-κBp65 protein expression levels in the hippocampus of MCAO/R rats.</p><p><strong>Conclusions: </strong>Fingolimod was found to reduce ischemic brain injury in a dose-dependent manner. Moreover, it was also found to alleviate inflammation following ischemic brain injury via the HMGB1/TLR4/NF‑κB signaling pathway.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"142"},"PeriodicalIF":2.5,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108151","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 Hypertension on Alzheimer's Disease: Updates in Pathophysiological and Neuroimaging Findings.","authors":"Si-Cheng Yan, Lu Liu, Gao-Li Fang, Shi-Ting Weng, Jun-Jun Wang, Lin Cheng, Ye-Jia Mo, Qi-Lun Lai, Yin-Xi Zhang, Tian-Yi Zhang, Pan-Pan Gai, Li-Ying Zhuang, Song Qiao","doi":"10.31083/j.jin2308143","DOIUrl":"https://doi.org/10.31083/j.jin2308143","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is recognized as the leading cause of dementia, imposing a significant economic toll on society. Despite the emergence of novel therapeutic approaches for AD, their efficacy and safety mandates further validation through rigorous clinical trials. In this context, hypertension (HTN) has garnered considerable attention as an amendable risk factor for AD. Research indicates that hypertension during midlife is associated with an elevated risk of AD in later years, influencing both the onset and progression of the disease. Nevertheless, the relationship between AD and hypertension in the later stages of life remains a subject of debate. Moreover, the consequences of blood pressure reduction on cognitive function, along with the optimal pharmacological interventions and therapeutic thresholds for hypertension, have emerged as pivotal areas of inquiry. This review synthesizes findings on epidemiology, neuroimaging, and biomarkers, and the effects of antihypertensive medications to elucidate the link between hypertension and cognitive performance. We particularly investigate how hypertension and AD are related by plasma sulfide dysregulation, offering possible indicators for future diagnosis and therapy.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 8","pages":"143"},"PeriodicalIF":2.5,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108147","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":"Differentially Expressed Proteins in the Serum of Elderly Patients Who Experienced Perioperative Neurocognitive Disorders Following Transurethral Resection of the Prostate.","authors":"Zhong-Sheng Wang, Yi-Fan Tang, Ting Liu, Qiu-Xia Xiao, Qiu-Yan Li, Hong-Yan Li, Qing Liu, Ying Zhang","doi":"10.31083/j.jin2306123","DOIUrl":"10.31083/j.jin2306123","url":null,"abstract":"<p><strong>Objective: </strong>Perioperative neurocognitive disorders (PND) are a group of prevalent neurological complications that often occur in elderly individuals following major or emergency surgical procedures. The etiologies are not fully understood. This study endeavored to investigate novel targets and prediction methods for the occurrence of PND.</p><p><strong>Methods: </strong>A total of 229 elderly patients diagnosed with prostatic hyperplasia who underwent transurethral resection of the prostate (TURP) combined with spinal cord and epidural analgesia were included in this study. The patients were divided into two groups, the PND group and non-PND group, based on the Z-score method. According to the principle of maintaining consistency between preoperative and intraoperative conditions, three patients from each group were randomly chosen for serum sample collection. isobaric tags for relative and absolute quantification (iTRAQ) proteomics technology was employed to analyze and identify the proteins that exhibited differential expression in the serum samples from the two groups. Bioinformatics analysis was performed on the proteins that exhibited differential expression.</p><p><strong>Results: </strong>Among the 1101 serum proteins analyzed in the PND and non-PND groups, eight differentially expressed proteins were identified in PND patients. Of these, six proteins showed up-regulation, while two proteins showed down-regulation. Further bioinformatics analysis of the proteins that exhibited differential expression revealed their predominant involvement in cellular biological processes, cellular component formation, as well as endocytosis and phagocytosis Additionally, these proteins were found to possess the RING domain of E3 ubiquitin ligase.</p><p><strong>Conclusion: </strong>The iTRAQ proteomics technique was employed to analyze the variation in protein expression in serum samples from patients with PND and those without PND. This study successfully identified eight proteins that exhibited differential expression levels between the two groups. Bioinformatics analysis indicates that proteins exhibiting differential expression are primarily implicated in the biological processes associated with microtubules. Investigating the microtubule formation process as it relates to neuroplasticity and synaptic formation may offer valuable insights for enhancing our comprehension and potential prevention of PND.</p><p><strong>Clinical trial registration: </strong>Registered (ChiCTR2000028836). Date (20190306).</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"123"},"PeriodicalIF":2.5,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468599","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":"Utilizing Phase Locking Value to Determine Neurofeedback Treatment Responsiveness in Attention Deficit Hyperactivity Disorder.","authors":"Mohammad Reza Yousefi, Nikoo Khanahmadi, Amin Dehghani","doi":"10.31083/j.jin2306121","DOIUrl":"https://doi.org/10.31083/j.jin2306121","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Neurofeedback is a non-invasive brain training technique used to enhance and treat hyperactivity disorder by altering the patterns of brain activity. Nonetheless, the extent of enhancement by neurofeedback varies among individuals/patients and many of them are irresponsive to this treatment technique. Therefore, several studies have been conducted to predict the effectiveness of neurofeedback training including the theta/beta protocol with a specific emphasize on slow cortical potential (SCP) before initiating treatment, as well as examining SCP criteria according to age and sex criteria in diverse populations. While some of these studies failed to make accurate predictions, others have demonstrated low success rates. This study explores functional connections within various brain lobes across different frequency bands of electroencephalogram (EEG) signals and the value of phase locking is used to predict the potential effectiveness of neurofeedback treatment before its initiation.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This study utilized EEG data from the Mendelian database. In this database, EEG signals were recorded during neurofeedback sessions involving 60 hyperactive students aged 7-14 years, irrespective of sex. These students were categorized into treatable and non-treatable. The proposed method includes a five-step algorithm. Initially, the data underwent preprocessing to reduce noise using a multi-stage filtering process. The second step involved extracting alpha and beta frequency bands from the preprocessed EEG signals, with a particular emphasis on the EEG recorded from sessions 10 to 20 of neurofeedback therapy. In the third step, the method assessed the disparity in brain signals between the two groups by evaluating functional relationships in different brain lobes using the phase lock value, a crucial data characteristic. The fourth step focused on reducing the feature space and identifying the most effective and optimal electrodes for neurofeedback treatment. Two methods, the probability index (&lt;i&gt;p&lt;/i&gt;-value) via a &lt;i&gt;t&lt;/i&gt;-test and the genetic algorithm, were employed. These methods showed that the optimal electrodes were in the frontal lobe and central cerebral cortex, notably channels C3, FZ, F4, CZ, C4, and F3, as they exhibited significant differences between the two groups. Finally, in the fifth step, machine learning classifiers were applied, and the results were combined to generate treatable and non-treatable labels for each dataset.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Among the classifiers, the support vector machine and the boosting method demonstrated the highest accuracy when combined. Consequently, the proposed algorithm successfully predicted the treatability of individuals with hyperactivity in a short time and with limited data, achieving an accuracy of 90.6% in the neurofeedback method. Additionally, it effectively identified key electrodes in neurofeedback treatment, reducing their number","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"121"},"PeriodicalIF":2.5,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468628","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":"Systematic Review and Metanalysis of the Expression of Blood-Based and Cerebrospinal Fluid-Based Biomarkers Related to Inflammatory Mediators in Neuropathic Pain.","authors":"Marina Sanz-Gonzalez, Miguel Molina-Alvarez, Carmen Rodriguez-Rivera, David Pascual, Carlos Goicoechea","doi":"10.31083/j.jin2306120","DOIUrl":"10.31083/j.jin2306120","url":null,"abstract":"<p><strong>Background: </strong>The understanding of neuropathic pain remains incomplete, highlighting the need for research on biomarkers for improved diagnosis and treatment. This review focuses on identifying potential biomarkers in blood and cerebrospinal fluid for neuropathic pain in different neuropathies.</p><p><strong>Methods: </strong>Searches were performed in six databases: PubMed, Web of Science, Scopus, Cochrane Library, EMBASE, and CINAHL. Included were observational studies, namely cross-sectional, cohort, and case-control, that evaluated quantitative biomarkers in blood or cerebrospinal fluid. Data were qualitatively synthesized, and meta-analyses were conducted using R. The study is registered with PROSPERO under the ID CRD42022323769.</p><p><strong>Results: </strong>The literature search resulted in 16 studies for qualitative and 12 for quantitative analysis, covering patients over 18 years of age with painful neuropathies. A total of 1403 subjects were analyzed, identifying no significant differences in levels of C-Reactive Protein (CRP), Interleukin-6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-alpha) between patients with and without pain. Despite the high inter-rater reliability and adequate bias assessment, the results suggest negligible differences in inflammatory biomarkers, with noted publication bias and heterogeneity among studies, indicating the need for further research.</p><p><strong>Conclusions: </strong>Our review underscores the complex nature of neuropathic pain and the challenges in identifying biomarkers, with no significant differences found in CRP, IL-6, and TNF-alpha levels between patients with and without pain. Despite methodological robustness, the results are limited by publication bias and heterogeneity. This emphasizes the need for further research to discover definitive biomarkers for improved diagnosis and personalized treatment of neuropathic pain.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"120"},"PeriodicalIF":2.5,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468627","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":"Antiepileptic and Neuroprotective Effects of <i>Rheum tanguticum</i> Root Extract on Trimethyltin-Induced Epilepsy and Neurodegeneration: <i>In Vivo</i> and <i>in Silico</i> Analyses.","authors":"Jae-Young Choi, Sohi Kang, Minh Nhat Tran, Sanghun Lee, Seung Mok Ryu, Sung-Wook Chae, Do-Hyun Kim, Ye Eun Lee, Sohee Jeong, Changjong Moon, Joong Sun Kim, Soong-In Lee","doi":"10.31083/j.jin2306122","DOIUrl":"https://doi.org/10.31083/j.jin2306122","url":null,"abstract":"<p><strong>Background: </strong><i>Rheum tanguticum</i> root, cataloged as \"<i>Daehwang</i>\" in the Korean Pharmacopeia, is rich in various anthraquinones known for their anti-inflammatory and antioxidant properties. Formulations containing <i>Daehwang</i> are traditionally employed for treating neurological conditions. This study aimed to substantiate the antiepileptic and neuroprotective efficacy of <i>R. tanguticum</i> root extract (RTE) against trimethyltin (TMT)-induced epileptic seizures and hippocampal neurodegeneration.</p><p><strong>Methods: </strong>The constituents of RTE were identified by ultra-performance liquid chromatography (UPLC). Experimental animals were grouped into the following five categories: control, TMT, and three TMT+RTE groups with dosages of 10, 30, and 100 mg/kg. Seizure severity was assessed daily for comparison between the groups. Brain tissue samples were examined to determine the extent of neurodegeneration and neuroinflammation using histological and molecular biology techniques. Network pharmacology analysis involved extracting herbal targets for <i>Daehwang</i> and disease targets for epilepsy from multiple databases. A protein-protein interaction network was built using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, and pivotal targets were determined by topological analysis. Enrichment analysis was performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) tool to elucidate the underlying mechanisms.</p><p><strong>Results: </strong>The RTE formulation was found to contain sennoside A, sennoside B, chrysophanol, emodin, physcion, (+)-catechin, and quercetin-3-O-glucuronoid. RTE effectively inhibited TMT-induced seizures at 10, 30, and 100 mg/kg dosages and attenuated hippocampal neuronal decay and neuroinflammation at 30 and 100 mg/kg dosages. Furthermore, RTE significantly reduced mRNA levels of tumor necrosis factor (<i>TNF-α</i>), glial fibrillary acidic protein (<i>GFAP</i>), and <i>c-fos</i> in hippocampal tissues. Network analysis revealed TNF, Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Protein c-fos (FOS), RAC-alpha serine/threonine-protein kinase (AKT1), and Mammalian target of rapamycin (mTOR) as the core targets. Enrichment analysis demonstrated significant involvement of <i>R. tanguticum</i> components in neurodegeneration (<i>p</i> = 4.35 × 10-5) and TNF signaling pathway (<i>p</i> = 9.94 × 10-5).</p><p><strong>Conclusions: </strong>The <i>in vivo</i> and <i>in silico</i> analyses performed in this study suggests that RTE can potentially modulate TMT-induced epileptic seizures and neurodegeneration. Therefore, <i>R. tanguticum</i> root is a promising herbal treatment option for antiepileptic and neuroprotective applications.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"122"},"PeriodicalIF":2.5,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468584","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":"Human NMO-IgG Induced Different Pathological and Immunological Changes in the CNS and Peripheral Tissues of Mice.","authors":"Weiwei Xiang, Shuwei Bai, Kan Wang, Jing Peng, Ze Wang, Lu Han, Chong Xie, Yangtai Guan","doi":"10.31083/j.jin2306119","DOIUrl":"10.31083/j.jin2306119","url":null,"abstract":"<p><strong>Objectives: </strong>The majority of neuromyelitis optica spectrum disorders (NMOSD) patients are seropositive for aquaporin-4 (AQP4)-specific antibodies [also named neuromyelitis optica immunoglobulin G antibodies (NMO-IgG)]. Although NMO-IgG can induce pathological changes in the central nervous system (CNS), the immunological changes in the CNS and peripheral tissue remain largely unknown. We investigated whether NMO-IgG binds to tissue expressing AQP4 and induces immunological changes in the peripheral tissue and CNS.</p><p><strong>Methods: </strong>C57BL/6 female mice were assigned into an NMOSD or control group. Pathological and immunological changes in peripheral tissue and CNS were measured by immunostaining and flow cytometry, respectively. Motor impairment was measured by open-field test.</p><p><strong>Results: </strong>We found that NMO-IgG did bind to astrocyte- and AQP4-expressing peripheral tissue, but induced glial fibrillary acidic protein and AQP4 loss only in the CNS. NMO-IgG induced the activation of microglia and modulated microglia polarization toward the classical (M1) phenotype, but did not affect innate or adaptive immune cells in the peripheral immune system, such as macrophages, neutrophils, Th17/Th1, or IL-10-producing B cells. In addition, NMOSD mice showed significantly less total distance traveled and higher immobility time in the open field.</p><p><strong>Conclusions: </strong>We found that injection of human NMO-IgG led to astrocytopathic lesions with microglial activation in the CNS. However, there were no significant pathological or immunological changes in the peripheral tissues.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"119"},"PeriodicalIF":2.5,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468603","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":"Chronic Alcohol Exposure Alters the Levels and Assembly of the Actin Cytoskeleton and Microtubules in the Adult Mouse Hippocampus.","authors":"Da-Peng Gao, Lu-Wan Wang, Dong-Lin Xie, Qiong Li, Zhi-Peng Yu, Zi-Hang Tang, Ke-Ke Cui, Yu Cai","doi":"10.31083/j.jin2306118","DOIUrl":"https://doi.org/10.31083/j.jin2306118","url":null,"abstract":"<p><strong>Background: </strong>Alcohol abuse, a prevalent global health issue, is associated with the onset of cognitive impairment and neurodegeneration. Actin filaments (F-actin) and microtubules (MTs) polymerized from monomeric globular actin (G-actin) and tubulin form the structural basis of the neuronal cytoskeleton. Precise regulation of the assembly and disassembly of these cytoskeletal proteins, and their dynamic balance, play a pivotal role in regulating neuronal morphology and function. Nevertheless, the effect of prolonged alcohol exposure on cytoskeleton dynamics is not fully understood. This study investigates the chronic effects of alcohol on cognitive ability, neuronal morphology and cytoskeleton dynamics in the mouse hippocampus.</p><p><strong>Methods: </strong>Mice were provided <i>ad libitum</i> access to 5% (v/v) alcohol in drinking water and were intragastrically administered 30% (v/v, 6.0 g/kg/day) alcohol for six weeks during adulthood. Cognitive functions were then evaluated using the Y maze, novel object recognition and Morris water maze tests. Hippocampal histomorphology was assessed through hematoxylin-eosin (HE) and Nissl staining. The polymerized and depolymerized states of actin cytoskeleton and microtubules were separated using two commercial assay kits and quantified by Western blot analysis.</p><p><strong>Results: </strong>Mice chronically exposed to alcohol exhibited significant deficits in spatial and recognition memory as evidenced by behavioral tests. Histological analysis revealed notable hippocampal damage and neuronal loss. Decreased ratios of F-actin/G-actin and MT/tubulin, along with reduced levels of polymerized F-actin and MTs, were found in the hippocampus of alcohol-treated mice.</p><p><strong>Conclusions: </strong>Our findings suggest that chronic alcohol consumption disrupted the assembly of the actin cytoskeleton and MTs in the hippocampus, potentially contributing to the cognitive deficits and pathological injury induced by chronic alcohol intoxication.</p>","PeriodicalId":16160,"journal":{"name":"Journal of integrative neuroscience","volume":"23 6","pages":"118"},"PeriodicalIF":2.5,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468598","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}