Synapse最新文献

{"title":"Sex and Chronic Stress Alter the Distribution of Corticotropin-Releasing Factor Receptor in Rat Hippocampus Following Oxycodone Conditioned Place Preference.","authors":"Dana N Silberstein, Zoha Baig, Batsheva Rubin, Fangmin Yu, Joshua Kogan, Jason D Gray, Yan Zhou, Teresa A Milner","doi":"10.1002/syn.70057","DOIUrl":"10.1002/syn.70057","url":null,"abstract":"<p><p>Corticotropin-releasing factor receptor 1 (CRFR1) plays a role in stress-induced hippocampal plasticity that can affect learning and memory processes including those important for addiction. Our prior work revealed sex differences in the distribution of CRFR1 within CA3 pyramidal cells and hilar interneurons in rats that could differentially affect associative learning processes in females and males, especially in response to chronic immobilization stress (CIS). Here, we examine the effect of oxycodone (Oxy) conditioned place preference (CPP) in unstressed and CIS adult female and male rats on the subcellular distribution of CRFR1 in CA3 pyramidal cells and dentate gyrus (DG) hilar interneurons using immuno-electron microscopy. After Oxy CPP, males compared to females had greater plasmalemmal-associated CRFR1 in CA3 pyramidal cell and DG interneuron dendrites, consistent with a greater binding capacity for corticotropin-releasing factor (CRF) in males. CIS alone resulted in increases in corticotropin-releasing hormone receptor 1 (Crhr1) mRNA in the pyramidal cell layer and stratum oriens of CA3 in males. Following CIS and Oxy CPP behavior, only females acquired CPP. Oxy CIS females compared to Oxy CIS males had more total CRFR1 in DG interneuron dendrites. Moreover, CRFR1 trafficked from the cytoplasm toward the plasmalemma in DG interneuron dendrites in CIS Oxy females, indicating a potential greater binding capacity for CIS Oxy females in this neuronal population. These findings along with prior studies suggest that changes in CRFR1 and opioid receptor trafficking in CIS females contribute to mechanisms that are associated with the development of Oxy CPP in CIS females, but not males.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 5","pages":"e70057"},"PeriodicalIF":2.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13519899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148832473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA MIAT Protects Against Sevoflurane-Induced Cognitive Dysfunction in Neonatal Rats via the miR-15b-5p/Ccnd1 Axis.","authors":"Xuewen Lu, Xinyi He, Zhenbin Zhan, Hai Chen, Jinguang Chen, Zhiwei Fan","doi":"10.1002/syn.70050","DOIUrl":"10.1002/syn.70050","url":null,"abstract":"<p><p>This study aimed to investigate the role and underlying mechanism of lncRNA MIAT in sevoflurane (Sev)-induced cognitive dysfunction in neonatal rats, thereby offering theoretical basis for clinical intervention. Seven-day-old Sprague-Dawley (SD) rats were chosen to construct a Sev-induced cognitive dysfunction model. Anxiety-like behavior and locomotor activity were assessed by the open field test (OFT), whereas cognitive function was evaluated using novel object recognition (NOR) test and Morris water maze (MWM) test. The expression levels of lncRNA MIAT, miR-15b-5p, and Ccnd1 were detected by RT-qPCR. The dual-luciferase reporter gene assay was carried out to validate the targeted binding relationships. Sev exposure led to a downregulation of lncRNA MIAT expression in rat hippocampus. lncRNA MIAT alleviated Sev-induced cognitive impairment, as manifested by increased central zone residence time in OFT, elevated recognition index (RI) in NOR test, shortened escape latency, increased platform crossings, and prolonged target quadrant residence time in MWM test. Mechanistically, lncRNA MIAT directly targeted miR-15b-5p and inhibited its expression. miR-15b-5p targeted Ccnd1 and suppressed its expression. Overexpression of miR-15b-5p or silencing of Ccnd1 reversed the neuroprotective effect of lncRNA MIAT. LncRNA MIAT ameliorates Sev-induced cognitive dysfunction in neonatal rats by sponging miR-15b-5p to upregulate Ccnd1 expression, which may serve as a potential target for preventing Sev-related neurotoxicity.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 4","pages":"e70050"},"PeriodicalIF":2.5,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148353627","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":"Ketamine Responsiveness of Mice Exhibiting Anorexia-Like Behavior Correlates With Synaptic AMPA Receptor Distribution.","authors":"Bridget Xu, Cassandra Carrasco, Yi-Wen Chen, Chiye Aoki","doi":"10.1002/syn.70046","DOIUrl":"10.1002/syn.70046","url":null,"abstract":"<p><p>Anorexia nervosa is a deadly eating disorder marked by extreme food restriction, compulsive exercise, and severe weight loss. In a prior study using the activity-based anorexia (ABA) animal model of anorexia nervosa, 30 mg/kg, but not 3 mg/kg, of ketamine reduced relapse vulnerability, measured as increased food intake, increased body weight (BW), and reduced excessive wheel running, though there were individual differences in responsiveness to treatment. This study investigated whether ketamine evoked sustained changes to AMPA receptors (AMPARs) at excitatory synapses of the prefrontal cortex (PFC), and whether they might correlate with individual differences in sustained behavioral improvements. Adolescent female mice that received 30 mg/kg (N = 8) or 3 mg/kg (N = 8) of ketamine underwent two cycles of ABA induction (ABA1 and ABA2), which included acclimation to a wheel preceding food restriction, with ABA2 modeling relapse. We analyzed the distributions of PFC AMPARs at synapses of pyramidal neurons (PNs) and of GABA interneurons (GABA-INs) using electron microscopy, with 10-nm immunogold to localize AMPARs. Increased AMPARs in the cytoplasm of PN synapses correlated with better BW retention during ABA2, as well as a reduction in excessive wheel running. Increased AMPARs in PN synapses' cytoplasm and GABA-INs synapses' postsynaptic density were associated with higher food intake during recovery. These correlations fit with a previous proposal that excitatory outflow from PFC to the GABA-INs in the dorsal raphe promotes feeding, while decreased excitatory outflow from PFC to dorsal medial striatum decreases hyperactivity during ABA, both of which contribute positively toward gain of resilience against ABA.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 3","pages":"e70046"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628771","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":"Structural Architecture and Evolutionary Conservation of Cerebellin-Mediated Trans-Synaptic Signaling.","authors":"Panfeng Zhao, Jian Yang, Jie Yang, Jinfeng Du","doi":"10.1002/syn.70045","DOIUrl":"10.1002/syn.70045","url":null,"abstract":"<p><p>The cerebellin (CBLN) family includes CBLN1, CBLN2, CBLN3, and CBLN4, which are important secreted glycoproteins that play roles in synaptogenesis and the maintenance and plasticity of synapses across various regions of the central nervous system (CNS). Generally known for their implications in cerebellar parallel fiber-Purkinje cell synapses, CBLNs also play a comprehensive role in synaptic regulation in the CNS. By forming trans-synaptic complexes with postsynaptic glutamate delta receptors (GluDs) and presynaptic neurexins (NRXNs), CBLNs significantly impact the synaptic specificity and potency. Each CBLN protein has its own expression signature and function. Current research points to a key role for CBLN1 in forming excitatory synapses, especially in the cerebellum, while CBLN2 is reported to regulate inhibitory synaptic transmission and serotonergic circuits. In addition, CBLN3 regulates synaptic stability and is associated with many neurodevelopmental problems. Apart from its role in the regulation of inhibitory synapse formation, CBLN4 is also linked to many neurodegenerative disorders. Dysfunction of pathways associated with CBLN signaling has been linked to several neuropsychiatric and neurological disorders, such as ataxia and schizophrenia. This review article compares existing data on the structure, expression, and functional properties of CBLN proteins, their roles in synapse organization, and their potential as therapeutic targets for neurological disease.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 3","pages":"e70045"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699445","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":"Effect of Healthy Aging on the Cytoarchitecture of Layer V Pyramidal Neurons in the Motor Cortex of Rats: A Golgi Study.","authors":"David González-Tapia, Nallely Vázquez-Hernández, Ignacio González-Burgos","doi":"10.1002/syn.70047","DOIUrl":"10.1002/syn.70047","url":null,"abstract":"<p><p>In recent decades, the rate of aging has increased significantly worldwide. Since both cognitive and motor performance decline during aging, they are considered indicators of this stage of normal development. Successful, healthy aging-not associated with pathology-is accompanied by a decline in motor skills due to the underlying anatomical and functional organization of the motor cortex. Deep-layer V neurons are thought to be the relay that translates afferent information to this cortical region and the organizers of the output of information that generates motor activity. Basal dendritic arborization was studied using the Sholl method, along with dendritic spine density and the amounts of distinct spine types in medial segments of primary dendrites in deep pyramidal neurons of layer V of the motor cortex of young (3-4 months) and aged (22-24 months), male Sprague-Dawley rats. Significant reductions in dendritic arborization and spine density were observed in the aged animals. Each spine type-thin, mushroom, stubby, and wide-existed in lower numbers than in the young animals. Results suggest both a reduction in the integrative capacity of synaptic stimuli by pyramidal cells and a downregulation in the processing of excitatory information. These findings could underlie the decline in the acquisition and maintenance of motor skills during healthy aging.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 3","pages":"e70047"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639894","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":"Measurement of Tau Protein and Aβ Amyloid Plaques in Postmortem Human Brains of Down Syndrome and Alzheimer's Disease by Using [¹²⁵I]IPPI and [¹²⁵I]IBETA Autoradiography.","authors":"Agnes P Biju, Fariha Karim, Deanna M Schafer, Stephanie A Sison, Christopher Liang, Elizabeth Head, Jogeshwar Mukherjee","doi":"10.1002/syn.70044","DOIUrl":"10.1002/syn.70044","url":null,"abstract":"<p><p>The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer's disease (AD) and Down syndrome (DS). Continuous developments of PET tracers as biomarkers can be supported by autoradiography to validate effectiveness and accuracy of binding properties that elucidate the pathophysiology of DSAD and AD. This in vitro comparative study evaluates [¹²⁵I]IPPI binding to tau and [¹²⁵I]IBETA binding to Aβ plaques in the frontal cortex (FCX) and temporal cortex (TCX) of postmortem human brain slices of AD (n = 5), DSAD (n = 5), and cognitively normal (CN) (n = 5) cases. With anti-tau and anti-Aβ immunostains confirming the presence of tau and Aβ plaques, [¹²⁵I]IPPI and [¹²⁵I]IBETA binding in autoradiographic images were significantly higher in DSAD and AD gray matter (GM) compared to CN. When comparing DSAD with AD, FCX and TCX GM binding was similar throughout DSAD and AD, except in FCX GM where there was 48% more [¹²⁵I]IPPI binding in DSAD than AD. In vitro drug inhibition studies revealed that [¹²⁵I]IPPI binding was significantly inhibited with increasing harmine concentrations (IC₅₀ = 115 nM) in DSAD FCX and TCX, but KuFal194, a DYRK1A drug, minimally inhibited [¹²⁵I]IPPI binding in the same cases. The GM/white matter ratios for DSAD ([¹²⁵I]IPPI = 4.1, [¹²⁵I]IBETA = 2.9) and AD ([¹²⁵I]IPPI = 4.2, [¹²⁵I]IBETA = 2.6) were significantly greater than CN ([¹²⁵I]IPPI = 1.3, [¹²⁵I]IBETA = 1.2). A positive correlation between [¹²⁵I]IPPI and [¹²⁵I]IBETA binding suggests a synergistic relationship between tau and Aβ plaque in DSAD and AD pathology. This study demonstrates that [¹²⁵I]IPPI and [¹²⁵I]IBETA may serve as novel radiotracers in both DSAD and AD to continue diagnostic investigations.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 2","pages":"e70044"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12993093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147469437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics Dissection of the Role of Ubiquitination Modification in Post-Stroke Neuroinflammation and Function Damage.","authors":"Peng Yao, Dan Li","doi":"10.1002/syn.70039","DOIUrl":"10.1002/syn.70039","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the role of ubiquitination in neuroinflammation and functional damage after stroke using multi-omics analysis, focusing on the pathways influenced by ubiquitination.</p><p><strong>Methods: </strong>Gene expression data related to stroke were collected from the GEO database. Differentially expressed genes were identified using the \"limma\" package in R. GO and KEGG enrichment analyses were performed to identify significant pathways. Ubiquitination data were integrated with differential gene data to identify genes with ubiquitination sites, focusing on those that bind to E3 ligases. Network analysis was conducted to examine the interactions among ubiquitin-modified proteins, and protein-RNA correlations were analyzed using data from proteomic analysis.</p><p><strong>Results: </strong>The analysis identified several inflammatory pathways significantly altered after stroke, including the NF-κB, TNF, and NOD-like receptor signaling pathways. A total of 113 genes with ubiquitination sites were found to be associated with E3 ligases and stroke-related genes. Among them, TRIM37 and TRIM25 emerged as key regulatory factors. Protein interaction network analysis revealed that ubiquitination modifications enhance neuroinflammation, leading to functional impairments. Post-translational modifications, indicated by higher protein stability, were observed in the proteins with the most ubiquitination sites, supporting their potential as therapeutic targets.</p><p><strong>Discussion: </strong>The study identifies TRIM37 and TRIM25 as crucial regulators of neuroinflammation through ubiquitination after stroke. These findings suggest that ubiquitination plays a significant role in stroke pathology and could serve as therapeutic targets for stroke treatment.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 2","pages":"e70039"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146165957","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":"Resveratrol Improves Fine Motor Performance and Attenuates Oxidative Stress, GFAP Reactivity, and Purkinje Cell Loss in the Cerebellum of Male Rats After 12, 18, and 24 Months of Treatment.","authors":"Daniel Juarez, Berenice Venegas, Dalia Molina-Romero, Ruben Vazquez-Roque, Jose Albino Moreno-Rodriguez, Fabian Galindo-Ramirez, Samuel Treviño, Jorge Guevara, Alfonso Diaz","doi":"10.1002/syn.70040","DOIUrl":"10.1002/syn.70040","url":null,"abstract":"<p><p>The cerebellum contributes to motor, cognitive, and affective functions that progressively decline with aging. The search for effective therapies to delay age-related degeneration has become a focus of the scientific community. Resveratrol, a natural polyphenol, exhibits neuroprotective properties through antioxidant and anti-inflammatory actions in different models of brain injury and aging. Here, we evaluated the effects of resveratrol on fine motor performance, oxidative stress, glial reactivity, and Purkinje cell survival in the cerebellum of male Wistar rats treated for 6, 12, 18, or 24 months. Three-month-old rats were randomly assigned to receive either vehicle (drinking water) or resveratrol (10 mg/kg, orally, daily by gavage between 8:00 and 10:00 a.m.). Fine motor skills were assessed using the balance beam test. Rats treated with resveratrol for 18 or 24 months showed improved motor coordination and fewer slips compared with controls. Histological analysis revealed less cellular disorganization and greater preservation of Purkinje cells after 12, 18, and 24 months of treatment. Nissl staining confirmed that resveratrol attenuated neuronal disintegration and preserved cerebellar architecture. Moreover, resveratrol significantly reduced GFAP immunoreactivity at 12, 18, and 24 months, indicating decreased astrocytic activation and inflammation. In conclusion, chronic resveratrol treatment exerted neuroprotective effects in the cerebellum, improving fine motor performance and reducing glial reactivity. These findings support resveratrol as a potential strategy to mitigate motor decline, inflammation, and cerebellar neurodegeneration associated with aging.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 2","pages":"e70040"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146114428","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":"Protective Role of miR-3909 Against Propofol-Induced Neurotoxicity Through the Regulation of Polymerase I and Transcript Release Factor.","authors":"Xiangyu Lu, Yuanzhu Li, Haitao Lou, Zhiqiang Feng, Chuancheng Zong","doi":"10.1002/syn.70041","DOIUrl":"10.1002/syn.70041","url":null,"abstract":"<p><p>Propofol (PPF), a commonly employed clinical anesthetic, has elicited growing concern due to its associated neurotoxic effects. However, the functional role and mechanistic insights of microRNA-3909 (miR-3909) in PPF-induced neurotoxicity remain unexplored. This study sought to elucidate the expression of miR-3909 and its underlying molecular mechanisms in the context of PPF-induced neurotoxicity. An in vitro model of  PPF neurotoxicity was established using SH-SY5Y cells (PPF-SH-SY5Y). Initial assessments via cell counting kit-8 (CCK-8) and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) demonstrated that treatment with 50 µM PPF significantly reduced cell viability and downregulated miR-3909 expression. Subsequent functional assays revealed that overexpression of miR-3909 effectively alleviated PPF-induced neurotoxicity, as evidenced by enhanced cell viability, suppression of apoptosis, reduced lactate dehydrogenase (LDH) release, and decreased reactive oxygen species (ROS) levels. Mechanistic investigations, including a dual-luciferase reporter assay, validated that miR-3909 directly targets and negatively regulates the expression of polymerase I and transcript release factor (PTRF). Notably, PTRF was significantly upregulated in PPF-SH-SY5Y cells, and overexpression of PTRF substantially counteracted the neuroprotective effects mediated by miR-3909. Collectively, these findings indicate that miR-3909 alleviates propofol-induced neurotoxicity by targeting PTRF, thereby providing a potential therapeutic target for this condition.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 2","pages":"e70041"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147322040","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":"Sevoflurane Triggers Glial Cell Damage Through BLACAT1/miR-361-3p Axis Resulting in Cognitive Impairment.","authors":"Jipeng Wen, Feiyu Long, Xiaoying Wang","doi":"10.1002/syn.70043","DOIUrl":"10.1002/syn.70043","url":null,"abstract":"<p><p>To investigate the regulatory mechanism of BLACAT1 expression in sevoflurane (Sev)-induced neuronal cell injury. An in vitro model was created by treating microglial cell lines with 3% Sev. An in vivo model was created by administering 2.2% Sev gas inhalation to mice for three consecutive days. Learning and memory capacity was assessed using the Morris water maze test. Gene expression was detected via RT-qPCR, while cellular functional alterations were observed through CCK-8 assays and flow cytometry. ELISA monitored inflammatory cytokine levels, while assay kits assessed oxidative stress marker expression. Dual luciferase reporter assay and RNA immunoprecipitation validated gene-target relationships. Treatment with Sev increased BLACAT1 levels in microglia and mouse hippocampi, while reducing the expression of miR-361-3p. Transfection with si-BLACAT1 counteracted the inhibitory effects of Sev on cell proliferation while reducing inflammatory and oxidative stress levels. miR-361-3p was a downstream target of BLACAT1, with miR inhibitor counteracting si-BLACAT1's protective effects on damaged neurons. Furthermore, Sev treatment impaired learning and memory functions in the mouse hippocampus, as evidenced by prolonged escape latency and fewer platform crossings during the original platform phase. BLACAT1 participates in Sev-induced glial cell injury via miR-361-3p, leading to hippocampal cognitive dysfunction.</p>","PeriodicalId":22131,"journal":{"name":"Synapse","volume":"80 2","pages":"e70043"},"PeriodicalIF":2.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147345011","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}