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Exosomal MiRNA Therapy for Central Nervous System Injury Diseases. 外泌体MiRNA治疗中枢神经系统损伤疾病。
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-12-09 DOI: 10.1007/s10571-024-01522-0
Cui Chang, Liang Weiping, Chen Jibing

Central nervous system diseases include central nervous system injury diseases, neurodegenerative diseases, and other conditions. MicroRNAs (miRNAs) are important regulators of gene expression, with therapeutic potential in modulating genes, pathways, and cells associated with central nervous system injury diseases. This article comprehensively reviews the therapeutic role of exosomal miRNAs in various central nervous system injury diseases, including traumatic brain injury, ischemic stroke, intracerebral hemorrhage, optic nerve injury, and spinal cord injury. This review covers the pathophysiology, animal models, miRNA transfection, administration methods, behavioral tests for evaluating treatment efficacy, and the mechanisms of action of miRNA-based therapies. Finally, this article discusses the future directions of miRNA therapy for central nervous system injury diseases.

中枢神经系统疾病包括中枢神经系统损伤性疾病、神经退行性疾病等。MicroRNAs (miRNAs)是基因表达的重要调控因子,在调节与中枢神经系统损伤疾病相关的基因、通路和细胞方面具有治疗潜力。本文全面综述了外泌体mirna在各种中枢神经系统损伤疾病中的治疗作用,包括外伤性脑损伤、缺血性卒中、脑出血、视神经损伤和脊髓损伤。本文综述了以miRNA为基础的治疗方法的病理生理学、动物模型、miRNA转染、给药方法、评估治疗效果的行为试验以及作用机制。最后,本文对miRNA治疗中枢神经系统损伤疾病的未来发展方向进行了展望。
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引用次数: 0
Identification of miRNA-TF Regulatory Pathways Related to Diseases from a Neuroendocrine-Immune Perspective. 从神经内分泌免疫角度鉴定与疾病相关的miRNA-TF调控通路
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-12-04 DOI: 10.1007/s10571-024-01510-4
Chengyi Wang, Meitao Wu, Ziyang Wang, Xiaoliang Wu, Hao Yuan, Shuo Jiang, Gen Li, Rifang Lan, Qiuping Wang, Guangde Zhang, Yingli Lv, Hongbo Shi

The neuroendocrine-immune (NEI) network is fundamental for maintaining body's homeostasis and health. While the roles of microRNAs (miRNAs) and transcription factors (TFs) in disease processes are well-established, their synergistic regulation within the NEI network has yet to be elucidated. In this study, we constructed a background NEI-related miRNA-TF regulatory network (NEI-miRTF-N) by integrating NEI signaling molecules (including miRNAs, genes, and TFs) and identifying miRNA-TF feed-forward loops. Our analysis reveals that the number of immune signaling molecules is the highest and suggests potential directions for signal transduction, primarily from the nervous system to both the endocrine and immune systems, as well as from the endocrine system to the immune system. Furthermore, disease-specific NEI-miRTF-Ns for depression, Alzheimer's disease (AD) and dilated cardiomyopathy (DCM) were constructed based on the known disease molecules and significantly differentially expressed (SDE) molecules. Additionally, we proposed a novel method using depth-first-search algorithm for identifying significantly dysregulated NEI-related miRNA-TF regulatory pathways (NEI-miRTF-Ps) and verified their reliability from multiple perspectives. Our study provides an effective approach for identifying disease-specific NEI-miRTF-Ps and offers new insights into the synergistic regulation of miRNAs and TFs within the NEI network. Our findings provide information for new therapeutic strategies targeting these regulatory pathways.

神经内分泌免疫(NEI)网络是维持机体内稳态和健康的基础。虽然microRNAs (miRNAs)和转录因子(tf)在疾病过程中的作用已经确立,但它们在NEI网络中的协同调节尚未阐明。本研究通过整合NEI信号分子(包括mirna、基因和tf),鉴定miRNA-TF前馈回路,构建了NEI相关miRNA-TF背景调控网络(NEI- mirtf - n)。我们的分析表明,免疫信号分子的数量是最高的,并提示信号转导的潜在方向,主要是从神经系统到内分泌和免疫系统,以及从内分泌系统到免疫系统。此外,基于已知的疾病分子和显著差异表达(SDE)分子,构建了抑郁症、阿尔茨海默病(AD)和扩张型心肌病(DCM)的疾病特异性NEI-miRTF-Ns。此外,我们提出了一种使用深度优先搜索算法识别显著失调的nei相关miRNA-TF调控通路(NEI-miRTF-Ps)的新方法,并从多个角度验证了其可靠性。我们的研究提供了一种识别疾病特异性NEI- mirtf - ps的有效方法,并为NEI网络中mirna和tf的协同调节提供了新的见解。我们的发现为针对这些调控途径的新治疗策略提供了信息。
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引用次数: 0
TMEM16A Activation Inhibits Autophagy in Dorsal Root Ganglion Cells, Which is Associated with the p38 MAPK/mTOR Pathway. TMEM16A激活抑制背根神经节细胞自噬,这与p38 MAPK/mTOR通路有关
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-12-04 DOI: 10.1007/s10571-024-01507-z
Shuyun Yang, Hui Shang, Yuruo Zhang, Jingsong Qiu, Zheyi Guo, Yong Ma, Yuhang Lan, Shaoyang Cui, Hongshuang Tong, Guocai Li

Transmembrane member 16A (TMEM16A) exhibits a negative correlation with autophagy, though the underlying mechanism remains elusive. This study investigates the mechanism between TMEM16A and autophagy by inducing autophagy in DRG neuronal cells using Rapamycin. Results indicated that TMEM16A interference augmented cell viability and reduced Rapamycin-induced apoptosis. Autophagosome formation increased with TMEM16A interference but decreased upon overexpression. A similar increase in autophagosomes was observed with SB203580 treatment. Furthermore, TMEM16A interference suppressed Rapamycin-induced gene and protein expression of p38 MAPK and mTOR, whereas overexpression had the opposite effect. These findings suggest that TMEM16A activation inhibits autophagy in DRG cells, which is associated with the p38 MAPK/mTOR pathway, offering a potential target for mitigating neuropathic pain (NP).

跨膜成员16A (TMEM16A)与自噬呈负相关,但其潜在机制尚不清楚。本研究通过使用雷帕霉素诱导DRG神经元细胞自噬来探讨TMEM16A与自噬之间的机制。结果表明,TMEM16A干扰增强了细胞活力,减少了雷帕霉素诱导的细胞凋亡。自噬体的形成在TMEM16A干扰下增加,在过表达时减少。在SB203580处理下观察到类似的自噬体增加。此外,TMEM16A干扰抑制rapamycin诱导的p38 MAPK和mTOR的基因和蛋白表达,而过表达则相反。这些发现表明,TMEM16A激活抑制DRG细胞的自噬,这与p38 MAPK/mTOR通路有关,为减轻神经性疼痛(NP)提供了一个潜在的靶点。
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引用次数: 0
The Role of Extracellular Vesicles and Microparticles in Central Nervous System Disorders: Mechanisms, Biomarkers, and Therapeutic Potential. 细胞外囊泡和微粒在中枢神经系统疾病中的作用:机制、生物标志物和治疗潜力。
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-12-03 DOI: 10.1007/s10571-024-01518-w
Soroush Najdaghi, Delaram Narimani Davani, Hamed Fouladseresht, Narges Ebrahimi, Mark J M Sullman, Marjan Moradi, Nahid Eskandari

Microscopic, membranous vesicles known as extracellular vesicles (EVs) have been proposed to play a role in the mechanisms underlying central nervous system (CNS) diseases. EVs are secreted by a variety of cells, including myeloid, endothelial, microglial, oligodendroglial, and mesenchymal stem cells (MSCs). Body fluids such as plasma, urine, and cerebrospinal fluid (CSF) contain microparticles (MPs). The detection of MPs in CSF may indicate genetic or environmental susceptibility to conditions such as schizophrenia, schizoaffective disorder, and bipolar disorder. MPs of different origins can exhibit changes in specific biomarkers at various stages of the disease, aiding in the diagnosis and monitoring of neurological conditions. However, understanding the role and clinical applications of MPs is complicated by challenges such as their isolation and dual roles within the CNS. In this review, we discuss the history, characteristics, and roles of MPs in CNS diseases. We also provide practical insights for future research and highlight the challenges that obscure the therapeutic potential of MPs.

被称为细胞外囊泡(EVs)的微观膜性囊泡已被提出在中枢神经系统(CNS)疾病的机制中发挥作用。ev由多种细胞分泌,包括髓细胞、内皮细胞、小胶质细胞、少突胶质细胞和间充质干细胞(MSCs)。体液如血浆、尿液和脑脊液(CSF)含有微粒(MPs)。脑脊液中MPs的检测可能表明对精神分裂症、分裂情感性障碍和双相情感障碍等疾病的遗传或环境易感性。不同来源的MPs可以在疾病的不同阶段表现出特定生物标志物的变化,有助于诊断和监测神经系统疾病。然而,MPs的作用和临床应用由于它们在中枢神经系统中的孤立性和双重作用等挑战而变得复杂。在这篇综述中,我们讨论MPs的历史、特点和在中枢神经系统疾病中的作用。我们还为未来的研究提供了实用的见解,并强调了模糊MPs治疗潜力的挑战。
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引用次数: 0
Molecular and Cellular Foundations of Aging of the Brain: Anti-aging Strategies in Alzheimer's Disease. 大脑老化的分子和细胞基础:阿尔茨海默病的抗衰老策略》。
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-28 DOI: 10.1007/s10571-024-01514-0
Magdalena Dziewa, Magdalena Złotek, Mariola Herbet, Iwona Piątkowska-Chmiel

Alzheimer's disease (AD) is a condition characterized by the gradual degeneration of the nervous system that poses significant challenges to cognitive function and overall mental health. Given the increasing global life expectancy, there is an urgent need for effective strategies to prevent and manage Alzheimer's disease, with a particular focus on anti-aging interventions. Recent scientific advancements have unveiled several promising strategies for combating Alzheimer's disease (AD), ranging from lifestyle interventions to cutting-edge pharmacological treatments and therapies targeting the underlying biological processes of aging and AD. Regular physical exercise, cognitive engagement, a balanced diet, and social interaction serve as key pillars in maintaining brain health. At the same time, therapies target key pathological mechanisms of AD, such as amyloid-beta accumulation, tau abnormalities, neuroinflammation, mitochondrial dysfunction, and synaptic loss, offering potential breakthroughs in treatment. Moreover, cutting-edge innovations such as gene therapy, stem cell transplantation, and novel drug delivery systems are emerging as potential game-changers in the fight against AD. This review critically evaluates the latest research on anti-aging interventions and their potential in preventing and treating Alzheimer's disease (AD) by exploring the connections between aging mechanisms and AD pathogenesis. It provides a comprehensive analysis of both well-established and emerging strategies, while also identifying key gaps in current knowledge to guide future research efforts.

阿尔茨海默病(AD)是一种以神经系统逐渐退化为特征的疾病,对认知功能和整体心理健康构成重大挑战。随着全球人口寿命的延长,人们迫切需要有效的策略来预防和控制阿尔茨海默病,尤其是抗衰老干预措施。最近的科学进步揭示了几种很有希望的抗击阿尔茨海默病(AD)的策略,从生活方式干预到针对衰老和阿尔茨海默病潜在生物过程的尖端药物治疗和疗法,不一而足。有规律的体育锻炼、认知参与、均衡饮食和社交互动是保持大脑健康的关键支柱。与此同时,针对注意力缺失症关键病理机制的疗法,如淀粉样蛋白-β积累、tau异常、神经炎症、线粒体功能障碍和突触丧失等,为治疗提供了潜在的突破口。此外,基因治疗、干细胞移植和新型给药系统等前沿创新技术正在成为改变抗击AD的潜在手段。本综述通过探讨衰老机制与阿尔茨海默病发病机制之间的联系,对抗衰老干预措施的最新研究及其在预防和治疗阿尔茨海默病(AD)方面的潜力进行了批判性评估。它全面分析了成熟的和新兴的策略,同时还找出了当前知识中的关键差距,以指导未来的研究工作。
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引用次数: 0
Neuropathic Pain Induced by Spinal Cord Injury from the Glia Perspective and Its Treatment. 从胶质细胞角度看脊髓损伤引起的神经性疼痛及其治疗
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-28 DOI: 10.1007/s10571-024-01517-x
Ying Ye, Xinjin Su, Jun Tang, Chao Zhu

Regional neuropathic pain syndromes above, at, or below the site of spinal damage arise after spinal cord injury (SCI) and are believed to entail distinct pathways; nevertheless, they may share shared defective glial systems. Neuropathic pain after SCI is caused by glial cells, ectopic firing of neurons endings and their intra- and extracellular signaling mechanisms. One such mechanism occurs when stimuli that were previously non-noxious become so after the injury. This will exhibit a symptom of allodynia. Another mechanism is the release of substances by glia, which keeps the sensitivity of dorsal horn neurons even in regions distant from the site of injury. Here, we review, the models and identifications of SCI-induced neuropathic pain (SCI-NP), the mechanisms of SCI-NP related to glia, and the treatments of SCI-NP.

脊髓损伤(SCI)后,脊髓损伤部位上方、下方或下方会出现区域性神经病理性疼痛综合征,这些综合征被认为涉及不同的途径;然而,它们可能共享有缺陷的神经胶质细胞系统。脊髓损伤后的神经性疼痛是由神经胶质细胞、神经元末梢的异位发射及其细胞内和细胞外信号机制引起的。其中一种机制是当以前无痛的刺激在受伤后变得有痛。这将表现出异痛症的症状。另一种机制是神经胶质细胞释放物质,即使在远离损伤部位的区域也能保持背角神经元的敏感性。在此,我们回顾了 SCI 诱导的神经病理性疼痛(SCI-NP)的模型和鉴定、与神经胶质细胞有关的 SCI-NP 机制以及 SCI-NP 的治疗方法。
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引用次数: 0
The Role of Photobiomodulation to Modulate Ion Channels in the Nervous System: A Systematic Review. 光生物调制在调节神经系统离子通道中的作用:系统综述。
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-23 DOI: 10.1007/s10571-024-01513-1
Zhixin Zhang, Zhiyu Zhang, Peng Liu, Xinmiao Xue, Chi Zhang, Lili Peng, Weidong Shen, Shiming Yang, Fangyuan Wang

Photobiomodulation (PBM) is a safe and effective neurotherapy that modulates cellular pathways by altering cell membrane potentials, leading to beneficial biological effects such as anti-inflammatory and neuroregenerative responses. This review compiles studies from PubMed up to March 2024, investigating the impact of light at wavelengths ranging from 620 to 1270 nm on ion channels. Out of 330 articles screened, 19 met the inclusion criteria. Research indicates that PBM can directly affect various ion channels by influencing neurotransmitter synthesis in neighboring cells, impacting receptors like glutamate and acetylcholine, as well as potassium, sodium channels, and transient receptor potential channels. The diversity of studies hampers a comprehensive meta-analysis for evaluating treatment strategies effectively. This systematic review aims to explore the potential role of optoelectronic signal transduction in PBM, studying the neurobiological mechanisms and therapeutic significance of PBM on ion channels. However, the lack of uniformity in current treatment methods underscores the necessity of establishing standardized and reliable therapeutic approaches.

光生物调节(PBM)是一种安全有效的神经疗法,它通过改变细胞膜电位来调节细胞通路,从而产生有益的生物效应,如抗炎和神经再生反应。本综述汇编了 PubMed 上截至 2024 年 3 月的研究,这些研究调查了波长为 620 到 1270 纳米的光对离子通道的影响。在筛选出的 330 篇文章中,有 19 篇符合纳入标准。研究表明,PBM 可通过影响邻近细胞的神经递质合成、影响谷氨酸和乙酰胆碱等受体以及钾、钠通道和瞬时受体电位通道,直接影响各种离子通道。研究的多样性阻碍了对治疗策略进行有效评估的全面荟萃分析。本系统综述旨在探讨光电信号转导在 PBM 中的潜在作用,研究 PBM 对离子通道的神经生物学机制和治疗意义。然而,目前的治疗方法缺乏统一性,这凸显了建立标准化、可靠的治疗方法的必要性。
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引用次数: 0
The Role of Inflammatory Cascade and Reactive Astrogliosis in Glial Scar Formation Post-spinal Cord Injury. 炎症级联和反应性星形胶质细胞在脊髓损伤后胶质瘢痕形成中的作用
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-23 DOI: 10.1007/s10571-024-01519-9
Manini Bhatt, Muskan Sharma, Bodhisatwa Das

Reactive astrogliosis and inflammation are pathologic hallmarks of spinal cord injury. After injury, dysfunction of glial cells (astrocytes) results in glial scar formation, which limits neuronal regeneration. The blood-spinal cord barrier maintains the structural and functional integrity of the spinal cord and does not allow blood vessel components to leak into the spinal cord microenvironment. After the injury, disruption in the spinal cord barrier causes an imbalance of the immunological microenvironment. This triggers the process of neuroinflammation, facilitated by the actions of microglia, neutrophils, glial cells, and cytokines production. Recent work has revealed two phenotypes of astrocytes, A1 and A2, where A2 has a protective type, and A1 releases neurotoxins, further promoting glial scar formation. Here, we first describe the current understanding of the spinal cord microenvironment, both pre-, and post-injury, and the role of different glial cells in the context of spinal cord injury, which forms the essential update on the cellular and molecular events following injury. We aim to explore in-depth signaling pathways and molecular mediators that trigger astrocyte activation and glial scar formation. This review will discuss the activated signaling pathways in astrocytes and other glial cells and their collaborative role in the development of gliosis through inflammatory responses.

反应性星形胶质细胞增多和炎症是脊髓损伤的病理特征。损伤后,神经胶质细胞(星形胶质细胞)的功能障碍导致神经胶质细胞瘢痕形成,从而限制了神经元的再生。血液-脊髓屏障可保持脊髓结构和功能的完整性,不允许血管成分渗漏到脊髓微环境中。损伤后,脊髓屏障的破坏会导致免疫微环境失衡。小胶质细胞、中性粒细胞、神经胶质细胞的作用和细胞因子的产生促进了神经炎症过程。最近的研究揭示了星形胶质细胞的两种表型,即 A1 和 A2,其中 A2 具有保护性,而 A1 则释放神经毒素,进一步促进胶质疤痕的形成。在这里,我们首先描述目前对脊髓微环境(包括损伤前和损伤后)的理解,以及不同胶质细胞在脊髓损伤中的作用,这构成了损伤后细胞和分子事件的基本更新。我们旨在深入探讨引发星形胶质细胞活化和胶质疤痕形成的信号通路和分子介质。本综述将讨论星形胶质细胞和其他胶质细胞中被激活的信号通路,以及它们通过炎症反应在胶质病变发展过程中的协同作用。
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引用次数: 0
Rasopathy-Associated Mutation Ptpn11D61Y has Age-Dependent Effect on Synaptic Vesicle Recycling. Rasopathy相关突变Ptpn11D61Y对突触小泡再循环的影响与年龄有关
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-21 DOI: 10.1007/s10571-024-01505-1
Debarpan Guhathakurta, Franziska Selzam, Aneta Petrušková, Eva-Maria Weiss, Enes Yağız Akdaş, Carolina Montenegro-Venegas, Martin Zenker, Anna Fejtová

Rasopathies are genetic disorders often associated with developmental delay and intellectual disability. Noonan syndrome (NS) is one of the most common Rasopathies, caused by mutations in PTPN11 in more than 50% of cases. In mammalian neurons, PTPN11 controls the trafficking of postsynaptic glutamate receptors. This process is disrupted in neurons expressing PTPN11 variants associated with Rasopathies and is thought to contribute to the cognitive impairments in Noonan syndrome. Recent work revealed presynaptic impairments upon expression of RASopathy-linked PTPN11 variants in Drosophila. However, the presynaptic role of PTPN11 has not yet been addressed in mammals. Here, we investigated membrane trafficking of synaptic vesicles in cultured mouse cortical neurons expressing Rasopathy-associated PTPN11D61Y variant. We observed a significantly smaller readily releasable and total recycling pool of synaptic vesicles. The drop in synaptic vesicle release competence was accompanied by a decreased rate of SV retrieval. Interestingly, the presynaptic phenotype was evident in mature (DIV21) but not in immature (DIV12) neurons. Thus, our data reveal importance of balanced PTPN11 activity for normal trafficking of neurotransmitter-filled synaptic vesicles in the presynaptic ending of mature neurons.

拉索病是一种遗传性疾病,通常与发育迟缓和智力障碍有关。努南综合征(NS)是最常见的拉索病之一,50% 以上的病例是由 PTPN11 基因突变引起的。在哺乳动物神经元中,PTPN11 控制突触后谷氨酸受体的贩运。在表达与拉索病相关的 PTPN11 变体的神经元中,这一过程被破坏,并被认为是造成努南综合征认知障碍的原因。最近的研究发现,果蝇在表达与 RAS 病相关的 PTPN11 变体时会出现突触前损伤。然而,PTPN11 在哺乳动物中的突触前作用尚未得到研究。在这里,我们研究了在表达 Rasopathy 相关 PTPN11D61Y 变体的培养小鼠皮质神经元中突触小泡的膜贩运。我们观察到突触囊泡的易释放性和总循环池明显减少。突触小泡释放能力的下降伴随着 SV 回收率的降低。有趣的是,突触前表型在成熟(DIV21)神经元中很明显,而在未成熟(DIV12)神经元中却不明显。因此,我们的数据揭示了平衡的 PTPN11 活性对成熟神经元突触前末端神经递质填充突触小泡正常贩运的重要性。
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引用次数: 0
Wnt-5a Signaling Mediates Metaplasticity at Hippocampal CA3-CA1 Synapses in Mice. Wnt-5a信号介导小鼠海马CA3-CA1突触的变态反应
IF 3.6 4区 医学 Q3 CELL BIOLOGY Pub Date : 2024-11-13 DOI: 10.1007/s10571-024-01512-2
Jorge Parodi, Rodrigo G Mira, Marco Fuenzalida, Waldo Cerpa, Felipe G Serrano, Cheril Tapia-Rojas, Ataulfo Martinez-Torres, Nibaldo C Inestrosa

Wnt signaling plays a role in synaptic plasticity, but the specific cellular events and molecular components involved in Wnt signaling-mediated synaptic plasticity are not well defined. Here, we report a change in the threshold required to induce synaptic plasticity that facilitates the induction of long-term potentiation (LTP) and inhibits the induction of long-term depression (LTD) during brief exposure to the noncanonical ligand Wnt-5a. Both effects are related to the metaplastic switch of hippocampal CA3-CA1 synaptic transmission, a complex mechanism underlying the regulation of the threshold required to induce synaptic plasticity and of synaptic efficacy. We observed an early increase in the amplitude of field excitatory postsynaptic potentials (fEPSPs) that persisted over time, including after washout. The first phase involves an increase in the fEPSP amplitude that is required to trigger a spontaneous second phase that depends on Jun N-terminal kinase (JNK) and N-methyl D-aspartate receptor (NMDAR) activity. These changes are prevented by treatment with secreted frizzled-related protein 2 (sFRP-2), an endogenous antagonist of Wnt ligands. Here, we demonstrate the contribution of Wnt-5a signaling to a process associated with metaplasticity at CA3-CA1 synapses that favors LTP over LTD.

Wnt信号在突触可塑性中发挥作用,但Wnt信号介导的突触可塑性所涉及的特定细胞事件和分子成分尚未得到很好的界定。在这里,我们报告了诱导突触可塑性所需的阈值的变化,这种变化在短暂暴露于非经典配体 Wnt-5a 的过程中促进了长期延时(LTP)的诱导,并抑制了长期抑制(LTD)的诱导。这两种效应都与海马 CA3-CA1 突触传递的元突变开关有关,这是一种调节诱导突触可塑性所需的阈值和突触效能的复杂机制。我们观察到场兴奋突触后电位(fEPSPs)振幅的早期增加,这种增加随着时间的推移而持续,包括在冲洗之后。第一阶段包括 fEPSP 振幅的增加,它是触发自发的第二阶段所必需的,第二阶段取决于 Jun N-terminal kinase (JNK) 和 N-methyl D-aspartate receptor (NMDAR) 的活性。用Wnt配体的内源性拮抗剂分泌型frizzled相关蛋白2(sFRP-2)处理可阻止这些变化。在这里,我们证明了 Wnt-5a 信号传导对 CA3-CA1 突触的变态反应过程的贡献,该过程有利于 LTP 而非 LTD。
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引用次数: 0
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