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Genetic approaches to elucidating cortical and hippocampal GABAergic interneuron diversity 阐明大脑皮层和海马 GABA 能中间神经元多样性的遗传方法
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-24 DOI: 10.3389/fncel.2024.1414955
Robert Machold, Bernardo Rudy
GABAergic interneurons (INs) in the mammalian forebrain represent a diverse population of cells that provide specialized forms of local inhibition to regulate neural circuit activity. Over the last few decades, the development of a palette of genetic tools along with the generation of single-cell transcriptomic data has begun to reveal the molecular basis of IN diversity, thereby providing deep insights into how different IN subtypes function in the forebrain. In this review, we outline the emerging picture of cortical and hippocampal IN speciation as defined by transcriptomics and developmental origin and summarize the genetic strategies that have been utilized to target specific IN subtypes, along with the technical considerations inherent to each approach. Collectively, these methods have greatly facilitated our understanding of how IN subtypes regulate forebrain circuitry via cell type and compartment-specific inhibition and thus have illuminated a path toward potential therapeutic interventions for a variety of neurocognitive disorders.
哺乳动物前脑中的 GABA 能中间神经元(IN)代表了一个多样化的细胞群体,它们提供专门的局部抑制形式来调节神经回路的活动。在过去的几十年里,随着单细胞转录组数据的产生,一系列遗传学工具的开发开始揭示 IN 多样性的分子基础,从而为深入了解不同 IN 亚型如何在前脑中发挥作用提供了依据。在这篇综述中,我们概述了由转录组学和发育起源所定义的大脑皮层和海马 IN 种群的新情况,并总结了针对特定 IN 亚型所采用的遗传策略,以及每种方法固有的技术注意事项。总之,这些方法极大地促进了我们对 IN 亚型如何通过细胞类型和区室特异性抑制调节前脑回路的理解,从而为各种神经认知障碍的潜在治疗干预指明了道路。
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引用次数: 0
Oligodendrocyte precursor cell-derived exosomes combined with cell therapy promote clinical recovery by immunomodulation and gliosis attenuation 少突胶质前体细胞衍生的外泌体与细胞疗法相结合,通过免疫调节和减轻胶质病变促进临床康复
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-23 DOI: 10.3389/fncel.2024.1413843
Sarah Ingrid Pinto Santos, Santiago José Ortiz-Peñuela, Alessandro de Paula Filho, Ana Laura Midori Rossi Tomiyama, Lilian de Oliveira Coser, Juliano Coelho da Silveira, Daniele dos Santos Martins, Adriano Polican Ciena, Alexandre Leite Rodrigues de Oliveira, Carlos Eduardo Ambrósio
Multiple sclerosis is a chronic inflammatory disease of the central nervous system characterized by autoimmune destruction of the myelin sheath, leading to irreversible and progressive functional deficits in patients. Pre-clinical studies involving the use of neural stem cells (NSCs) have already demonstrated their potential in neuronal regeneration and remyelination. However, the exclusive application of cell therapy has not proved sufficient to achieve satisfactory therapeutic levels. Recognizing these limitations, there is a need to combine cell therapy with other adjuvant protocols. In this context, extracellular vesicles (EVs) can contribute to intercellular communication, stimulating the production of proteins and lipids associated with remyelination and providing trophic support to axons. This study aimed to evaluate the therapeutic efficacy of the combination of NSCs and EVs derived from oligodendrocyte precursor cells (OPCs) in an animal model of multiple sclerosis. OPCs were differentiated from NSCs and had their identity confirmed by gene expression analysis and immunocytochemistry. Exosomes were isolated by differential ultracentrifugation and characterized by Western, transmission electron microscopy and nanoparticle tracking analysis. Experimental therapy of C57BL/6 mice induced with experimental autoimmune encephalomyelitis (EAE) were grouped in control, treated with NSCs, treated with OPC-derived EVs and treated with a combination of both. The treatments were evaluated clinically using scores and body weight, microscopically using immunohistochemistry and immunological profile by flow cytometry. The animals showed significant clinical improvement and weight gain with the treatments. However, only the treatments involving EVs led to immune modulation, changing the profile from Th1 to Th2 lymphocytes. Fifteen days after treatment revealed a reduction in reactive microgliosis and astrogliosis in the groups treated with EVs. However, there was no reduction in demyelination. The results indicate the potential therapeutic use of OPC-derived EVs to attenuate inflammation and promote recovery in EAE, especially when combined with cell therapy.
多发性硬化症是中枢神经系统的一种慢性炎症性疾病,其特点是髓鞘受到自身免疫性破坏,导致患者出现不可逆转的进行性功能障碍。使用神经干细胞(NSCs)进行的临床前研究已经证明了它们在神经元再生和髓鞘再形成方面的潜力。然而,仅应用细胞疗法还不足以达到令人满意的治疗水平。认识到这些局限性,有必要将细胞疗法与其他辅助方案相结合。在这种情况下,细胞外囊泡(EVs)可以促进细胞间的交流,刺激与再髓鞘化相关的蛋白质和脂质的产生,并为轴突提供营养支持。本研究旨在评估在多发性硬化症动物模型中,将少突胶质前体细胞(OPCs)提取的NSCs和EVs结合使用的疗效。OPCs 从 NSCs 分化而来,并通过基因表达分析和免疫细胞化学确认了其身份。通过差速超速离心法分离出外泌体,并通过Western、透射电子显微镜和纳米颗粒追踪分析对其进行鉴定。对诱发实验性自身免疫性脑脊髓炎(EAE)的 C57BL/6 小鼠的实验治疗分为对照组、NSCs 治疗组、OPC 衍生 EVs 治疗组和两者结合治疗组。临床上使用评分和体重对治疗进行评估,显微镜下使用免疫组化,流式细胞术对免疫学特征进行评估。动物的临床症状明显改善,体重增加。不过,只有使用 EVs 的治疗才会导致免疫调节,使 Th1 淋巴细胞变为 Th2 淋巴细胞。治疗十五天后发现,在使用EVs治疗的组中,反应性小胶质细胞和星形胶质细胞减少。不过,脱髓鞘现象并未减少。这些结果表明,OPC衍生的EVs具有潜在的治疗作用,可减轻炎症反应并促进EAE的恢复,尤其是在与细胞疗法相结合时。
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引用次数: 0
A novel histone deacetylase inhibitor W2A-16 improves the barrier integrity in brain vascular endothelial cells 新型组蛋白去乙酰化酶抑制剂 W2A-16 可改善脑血管内皮细胞屏障的完整性
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-19 DOI: 10.3389/fncel.2024.1368018
Yasuteru Inoue, Yingxue Ren, Shuwen Zhang, Michael Bamkole, Naeyma N. Islam, Manikandan Selvaraj, Wenyan Lu, Thomas R. Caulfield, Yonghe Li, Takahisa Kanekiyo
The maturation of brain microvascular endothelial cells leads to the formation of a tightly sealed monolayer, known as the blood–brain barrier (BBB). The BBB damage is associated with the pathogenesis of age-related neurodegenerative diseases including vascular cognitive impairment and Alzheimer’s disease. Growing knowledge in the field of epigenetics can enhance the understanding of molecular profile of the BBB and has great potential for the development of novel therapeutic strategies or targets to repair a disrupted BBB. Histone deacetylases (HDACs) inhibitors are epigenetic regulators that can induce acetylation of histones and induce open chromatin conformation, promoting gene expression by enhancing the binding of DNA with transcription factors. We investigated how HDAC inhibition influences the barrier integrity using immortalized human endothelial cells (HCMEC/D3) and the human induced pluripotent stem cell (iPSC)-derived brain vascular endothelial cells. The endothelial cells were treated with or without a novel compound named W2A-16. W2A-16 not only activates Wnt/β-catenin signaling but also functions as a class I HDAC inhibitor. We demonstrated that the administration with W2A-16 sustained barrier properties of the monolayer of endothelial cells, as evidenced by increased trans-endothelial electrical resistance (TEER). The BBB-related genes and protein expression were also increased compared with non-treated controls. Analysis of transcript profiles through RNA-sequencing in hCMEC/D3 cells indicated that W2A-16 potentially enhances BBB integrity by influencing genes associated with the regulation of the extracellular microenvironment. These findings collectively propose that the HDAC inhibition by W2A-16 plays a facilitating role in the formation of the BBB. Pharmacological approaches to inhibit HDAC may be a potential therapeutic strategy to boost and/or restore BBB integrity.
脑微血管内皮细胞成熟后会形成一个紧密密封的单层,即血脑屏障(BBB)。血脑屏障损伤与血管性认知障碍和阿尔茨海默病等与年龄相关的神经退行性疾病的发病机制有关。表观遗传学领域不断增长的知识可以加深人们对 BBB 分子特征的了解,并具有开发新型治疗策略或靶点以修复被破坏的 BBB 的巨大潜力。组蛋白去乙酰化酶(HDACs)抑制剂是一种表观遗传调节剂,可诱导组蛋白乙酰化并诱导染色质开放构象,通过增强 DNA 与转录因子的结合促进基因表达。我们使用永生化人内皮细胞(HCMEC/D3)和诱导多能干细胞(iPSC)衍生的脑血管内皮细胞研究了 HDAC 抑制如何影响屏障完整性。使用或不使用一种名为 W2A-16 的新型化合物处理内皮细胞。W2A-16 不仅能激活 Wnt/β-catenin 信号转导,而且还是一种 I 类 HDAC 抑制剂。我们证实,服用 W2A-16 能维持内皮细胞单层的屏障特性,表现为跨内皮电阻(TEER)的增加。与未经处理的对照组相比,与 BBB 相关的基因和蛋白质表达也有所增加。通过对 hCMEC/D3 细胞中的 RNA 序列进行转录谱分析表明,W2A-16 有可能通过影响与细胞外微环境调控相关的基因来增强 BBB 的完整性。这些发现共同表明,W2A-16 对 HDAC 的抑制在 BBB 的形成过程中起到了促进作用。抑制 HDAC 的药理方法可能是促进和/或恢复 BBB 完整性的潜在治疗策略。
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引用次数: 0
GABAA receptors and neuroligin 2 synergize to promote synaptic adhesion and inhibitory synaptogenesis GABAA 受体和神经胶质蛋白 2 协同促进突触粘附和抑制性突触生成
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-18 DOI: 10.3389/fncel.2024.1423471
Yusheng Sui, Martin Mortensen, Banghao Yuan, Martin W. Nicholson, Trevor G. Smart, Jasmina N. Jovanovic
GABAA receptors (γ-aminobutyric acid-gated receptors type A; GABAARs), the major structural and functional postsynaptic components of inhibitory synapses in the mammalian brain, belong to a family of GABA-gated Cl/HCO3 ion channels. They are assembled as heteropentamers from a family of subunits including: α (1–6), β(1–3), γ(1–3), δ, ε, π, θ and ρ(1–3). GABAARs together with the postsynaptic adhesion protein Neuroligin 2 (NL2) and many other pre- and post-synaptic proteins guide the initiation and functional maturation of inhibitory GABAergic synapses. This study examined how GABAARs and NL2 interact with each other to initiate the formation of synapses. Two functionally distinct GABAAR subtypes, the synaptic type α2β2γ2-GABAARs versus extrasynaptic type α4β3δ-GABAARs were expressed in HEK293 cells alone or together with NL2 and co-cultured with striatal GABAergic medium spiny neurons to enable innervation of HEK293 cells by GABAergic axons. When expressed alone, only the synaptic α2β2γ2-GABAARs induced innervation of HEK293 cells. However, when GABAARs were co-expressed with NL2, the effect on synapse formation exceeded the individual effects of these proteins indicating a synergistic interaction, with α2β2γ2-GABAAR/NL2 showing a significantly greater synaptogenic activity than α4β3δ-GABAAR/NL2 or NL2 alone. To investigate the molecular basis of this interaction, different combinations of GABAAR subunits and NL2 were co-expressed, and the degree of innervation and synaptic activity assessed, revealing a key role of the γ2 subunit. In biochemical assays, the interaction between NL2 and α2β2γ2-GABAAR was established and mapped to the large intracellular domain of the γ2 subunit.
GABAA 受体(γ-氨基丁酸门控受体 A 型;GABAARs)是哺乳动物大脑抑制性突触的主要结构和功能性突触后成分,属于 GABA 门控 Cl-/HCO3- 离子通道家族。它们是由α(1-6)、β(1-3)、γ(1-3)、δ、ε、π、θ 和 ρ(1-3)等一系列亚基组成的异源五聚体。GABAARs 与突触后粘附蛋白 Neuroligin 2(NL2)及其他许多突触前后蛋白一起引导抑制性 GABA 能突触的启动和功能成熟。本研究探讨了 GABAARs 和 NL2 如何相互作用以启动突触的形成。研究人员在HEK293细胞中单独或与NL2一起表达了两种功能不同的GABAAR亚型,即突触型α2β2γ2-GABAARs和突触外型α4β3δ-GABAARs,并与纹状体GABA能中棘神经元共同培养,使GABA能轴突能支配HEK293细胞。单独表达时,只有突触α2β2γ2-GABAARs能诱导HEK293细胞神经支配。然而,当 GABAARs 与 NL2 共同表达时,对突触形成的影响超过了这些蛋白的单独作用,这表明存在一种协同作用,α2β2γ2-GABAAR/NL2 的突触生成活性明显高于 α4β3δ-GABAAR/NL2 或 NL2 本身。为了研究这种相互作用的分子基础,我们共同表达了 GABAAR 亚基和 NL2 的不同组合,并评估了神经支配和突触活性的程度,结果显示 γ2 亚基发挥了关键作用。在生化试验中,确定了 NL2 与 α2β2γ2-GABAAR 之间的相互作用,并将其映射到 γ2 亚基的大胞内结构域。
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引用次数: 0
Electrophysiological activity pattern of mouse hippocampal CA1 and dentate gyrus under isoflurane anesthesia 异氟醚麻醉下小鼠海马 CA1 和齿状回的电生理活动模式
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-18 DOI: 10.3389/fncel.2024.1392498
Rui Wang, Linzhong Zhang, Xia Wang, Wen Li, Tingliang Jian, Pengcheng Yin, Xinzhi Wang, Qianwei Chen, Xiaowei Chen, Han Qin
General anesthesia can impact a patient’s memory and cognition by influencing hippocampal function. The CA1 and dentate gyrus (DG), serving as the primary efferent and gateway of the hippocampal trisynaptic circuit facilitating cognitive learning and memory functions, exhibit significant differences in cellular composition, molecular makeup, and responses to various stimuli. However, the effects of isoflurane-induced general anesthesia on CA1 and DG neuronal activity in mice are not well understood. In this study, utilizing electrophysiological recordings, we examined neuronal population dynamics and single-unit activity (SUA) of CA1 and DG in freely behaving mice during natural sleep and general anesthesia. Our findings reveal that isoflurane anesthesia shifts local field potential (LFP) to delta frequency and reduces the firing rate of SUA in both CA1 and DG, compared to wakefulness. Additionally, the firing rates of DG neurons are significantly lower than CA1 neurons during isoflurane anesthesia, and the recovery of theta power is slower in DG than in CA1 during the transition from anesthesia to wakefulness, indicating a stronger and more prolonged impact of isoflurane anesthesia on DG. This work presents a suitable approach for studying brain activities during general anesthesia and provides evidence for distinct effects of isoflurane anesthesia on hippocampal subregions.
全身麻醉会影响海马功能,从而影响患者的记忆和认知能力。CA1和齿状回(DG)是促进认知学习和记忆功能的海马三突触回路的主要传出和网关,它们在细胞组成、分子构成和对各种刺激的反应方面存在显著差异。然而,异氟醚诱导的全身麻醉对小鼠 CA1 和 DG 神经元活动的影响尚不十分清楚。在本研究中,我们利用电生理记录研究了自然睡眠和全身麻醉期间行为自由的小鼠 CA1 和 DG 的神经元群动态和单细胞活动(SUA)。我们的研究结果表明,与清醒时相比,异氟醚麻醉会使局部场电位(LFP)向δ频率移动,并降低CA1和DG中SUA的发射率。此外,在异氟烷麻醉期间,DG神经元的发射率明显低于CA1神经元,而且在从麻醉到清醒的过渡期间,DG的θ功率恢复比CA1慢,这表明异氟烷麻醉对DG的影响更强烈、更持久。这项研究为研究全身麻醉期间的大脑活动提供了一种合适的方法,并为异氟烷麻醉对海马亚区的不同影响提供了证据。
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引用次数: 0
Glial cells in the mammalian olfactory bulb 哺乳动物嗅球中的神经胶质细胞
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-16 DOI: 10.3389/fncel.2024.1426094
Dan Zhao, Meigeng Hu, Shaolin Liu
The mammalian olfactory bulb (OB), an essential part of the olfactory system, plays a critical role in odor detection and neural processing. Historically, research has predominantly focused on the neuronal components of the OB, often overlooking the vital contributions of glial cells. Recent advancements, however, underscore the significant roles that glial cells play within this intricate neural structure. This review discus the diverse functions and dynamics of glial cells in the mammalian OB, mainly focused on astrocytes, microglia, oligodendrocytes, olfactory ensheathing cells, and radial glia cells. Each type of glial contributes uniquely to the OB's functionality, influencing everything from synaptic modulation and neuronal survival to immune defense and axonal guidance. The review features their roles in maintaining neural health, their involvement in neurodegenerative diseases, and their potential in therapeutic applications for neuroregeneration. By providing a comprehensive overview of glial cell types, their mechanisms, and interactions within the OB, this article aims to enhance our understanding of the olfactory system's complexity and the pivotal roles glial cells play in both health and disease.
哺乳动物嗅球(OB)是嗅觉系统的重要组成部分,在气味检测和神经处理过程中发挥着关键作用。一直以来,研究主要集中在嗅球的神经元成分上,往往忽视了神经胶质细胞的重要贡献。然而,最近的研究进展强调了神经胶质细胞在这一错综复杂的神经结构中发挥的重要作用。这篇综述讨论了哺乳动物外显子中神经胶质细胞的各种功能和动态变化,主要集中在星形胶质细胞、小胶质细胞、少突胶质细胞、嗅鞘细胞和放射状胶质细胞。每种神经胶质细胞都对外显子的功能做出了独特的贡献,影响着从突触调节和神经元存活到免疫防御和轴突导向等各个方面。这篇综述介绍了它们在维持神经健康方面的作用、它们在神经退行性疾病中的参与,以及它们在神经再生治疗应用中的潜力。本文全面概述了神经胶质细胞的类型、机制以及在嗅觉器官中的相互作用,旨在加深我们对嗅觉系统复杂性以及神经胶质细胞在健康和疾病中的关键作用的理解。
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引用次数: 0
Frontiers | Peptain-1 blocks ischemia/reperfusion-induced retinal capillary degeneration in mice 前沿| Peptain-1可阻断缺血/再灌注诱导的小鼠视网膜毛细血管变性
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-16 DOI: 10.3389/fncel.2024.1441924
Mi-Hyun Nam, Armaan Dhillon, Rooban B. Nahomi, Noelle L. Carrillo, Clarinda S. Hougen, Ram H. Nagaraj
IntroductionNeurovascular degeneration results in vascular dysfunction, leakage, ischemia, and structural changes that can lead to significant visual impairment. We previously showed the protective effects of peptain-1, a 20 amino acid peptide derived from the αB-crystallin core domain, on retinal ganglion cells in two animal models of glaucoma. Here, we evaluated the ability of peptain-1 to block apoptosis of human retinal endothelial cells (HRECs) in vitro and retinal capillary degeneration in mice subjected to retinal ischemia/reperfusion (I/R) injury.MethodsHRECs were treated with either peptain-1 or scrambled peptides (200 μg/mL) for 3 h and a combination of proinflammatory cytokines (IFN-γ 20 ng/mL + TNF-α 20 ng/mL+ IL-1β 20 ng/mL) for additional 48 h. Apoptosis was measured with cleaved caspase-3 formation via western blot, and by TUNEL assay. C57BL/6J mice (12 weeks old) were subjected to I/R injury by elevating the intraocular pressure to 120 mmHg for 60 min, followed by reperfusion. Peptain-1 or scrambled peptide (0.5 μg) was intravitreally injected immediately after I/R injury and 7 days later. One microliter of PBS was injected as vehicle control, and animals were euthanized on day 14 post-I/R injury. Retinal capillary degeneration was assessed after enzyme digestion followed by periodic acid–Schiff staining.ResultsOur data showed that peptain-1 entered HRECs and blocked proinflammatory cytokine-mediated apoptosis. Intravitreally administered peptain-1 was distributed throughout the retinal vessels after 4 h. I/R injury caused retinal capillary degeneration. Unlike scrambled peptide, peptain-1 protected capillaries against I/R injury. Additionally, peptain-1 inhibited microglial activation and reduced proinflammatory cytokine levels in the retina following I/R injury.DiscussionOur study suggests that peptain-1 could be used as a therapeutic agent to prevent capillary degeneration and neuroinflammation in retinal ischemia.
导言神经血管变性会导致血管功能障碍、渗漏、缺血和结构变化,从而导致严重的视力损伤。我们以前曾在两种青光眼动物模型中发现过eptain-1对视网膜神经节细胞的保护作用,eptain-1是一种来自αB-结晶素核心结构域的20个氨基酸肽。在此,我们评估了eptain-1在体外阻断人视网膜内皮细胞(HRECs)凋亡的能力,以及在视网膜缺血/再灌注(I/R)损伤小鼠体内阻断视网膜毛细血管变性的能力。方法用eptain-1或加扰肽(200 μg/mL)处理HRECs 3小时,再用促炎细胞因子组合(IFN-γ 20 ng/mL + TNF-α 20 ng/mL+ IL-1β 20 ng/mL)处理48小时。将 C57BL/6J 小鼠(12 周大)的眼内压升高至 120 mmHg,使其受到 I/R 损伤 60 分钟,然后进行再灌注。在 I/R 损伤后立即和 7 天后静脉注射 Peptain-1 或加扰肽(0.5 μg)。动物在 I/R 损伤后第 14 天安乐死。结果我们的数据显示,培达-1能进入HRECs并阻止促炎细胞因子介导的细胞凋亡。玻璃体内给药的 peptain-1 在 4 小时后分布于整个视网膜血管。I/R 损伤导致视网膜毛细血管变性。与干扰肽不同,培达-1能保护毛细血管免受I/R损伤。讨论我们的研究表明,培达-1可作为一种治疗剂,用于预防视网膜缺血时的毛细血管变性和神经炎症。
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引用次数: 0
Assessment of corneal nerve regeneration after axotomy in a compartmentalized microfluidic chip model with automated 3D high resolution live-imaging 利用自动三维高分辨率实时成像技术,在分区微流控芯片模型中评估轴切断术后的角膜神经再生情况
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-15 DOI: 10.3389/fncel.2024.1417653
N. Bonneau, A. Potey, Frédéric Blond, Camille Guerin, C. Baudouin, J. Peyrin, F. Brignole-Baudouin, A. Réaux-Le Goazigo
Damage to the corneal nerves can result in discomfort and chronic pain, profoundly impacting the quality of life of patients. Development of novel in vitro method is crucial to better understand corneal nerve regeneration and to find new treatments for the patients. Existing in vitro models often overlook the physiology of primary sensory neurons, for which the soma is separated from the nerve endings.To overcome this limitation, our novel model combines a compartmentalized microfluidic culture of trigeminal ganglion neurons from adult mice with live–imaging and automated 3D image analysis offering robust way to assess axonal regrowth after axotomy.Physical axotomy performed by a two-second aspiration led to a reproducible 70% axonal loss and altered the phenotype of the neurons, increasing the number of substance P-positive neurons 72 h post-axotomy. To validate our new model, we investigated axonal regeneration after exposure to pharmacological compounds. We selected various targets known to enhance or inhibit axonal regrowth and analyzed their basal expression in trigeminal ganglion cells by scRNAseq. NGF/GDNF, insulin, and Dooku-1 (Piezo1 antagonist) enhanced regrowth by 81, 74 and 157%, respectively, while Yoda-1 (Piezo1 agonist) had no effect. Furthermore, SARM1-IN-2 (Sarm1 inhibitor) inhibited axonal regrowth, leading to only 6% regrowth after 72 h of exposure (versus 34% regrowth without any compound).Combining compartmentalized trigeminal neuronal culture with advanced imaging and analysis allowed a thorough evaluation of the extent of the axotomy and subsequent axonal regrowth. This innovative approach holds great promise for advancing our understanding of corneal nerve injuries and regeneration and ultimately improving the quality of life for patients suffering from sensory abnormalities, and related conditions.
角膜神经受损会导致不适和慢性疼痛,严重影响患者的生活质量。开发新型体外方法对于更好地了解角膜神经再生和为患者寻找新疗法至关重要。为了克服这一局限,我们的新型模型将成年小鼠三叉神经节神经元的分室微流控培养与实时成像和自动三维图像分析相结合,为评估轴突切断术后的轴突再生提供了可靠的方法。通过两秒钟的抽吸进行物理轴突切断,可重复地导致 70% 的轴突丢失,并改变了神经元的表型,增加了轴突切断后 72 小时 P 物质阳性神经元的数量。为了验证我们的新模型,我们研究了暴露于药理化合物后的轴突再生。我们选择了各种已知可促进或抑制轴突再生的靶点,并通过 scRNAseq 分析了它们在三叉神经节细胞中的基础表达。NGF/GDNF、胰岛素和Dooku-1(Piezo1拮抗剂)分别增强了轴突再生81%、74%和157%,而Yoda-1(Piezo1激动剂)则没有影响。此外,SARM1-IN-2(Sarm1 抑制剂)抑制轴突再生,在暴露 72 小时后仅有 6% 的轴突再生(而不使用任何化合物的情况下则有 34% 的轴突再生)。将三叉神经元分区培养与先进的成像和分析相结合,可以对轴突切断的程度和随后的轴突再生进行全面评估。这种创新方法有望促进我们对角膜神经损伤和再生的了解,并最终改善感觉异常和相关疾病患者的生活质量。
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引用次数: 0
Editorial: Space and neural cell: the impact of space environment on neurological function and their molecular mechanistic insights 社论:太空与神经细胞:太空环境对神经功能的影响及其分子机理认识
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-12 DOI: 10.3389/fncel.2024.1454014
Zixuan Chen, Zongjian Liu, Di Wu, Yulin Deng
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引用次数: 0
Microglia as potential key regulators in viral-induced neuroinflammation 小胶质细胞是病毒诱发神经炎症的潜在关键调控因子
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-11 DOI: 10.3389/fncel.2024.1426079
F. Ismail, Timo Jendrik Faustmann, P. Faustmann, Franco Corvace
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引用次数: 0
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