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Editorial: Cellular and molecular mechanisms in social and repetitive behaviours: a focus on cortico-striatal circuitry. 社论:社会和重复行为的细胞和分子机制:聚焦皮质纹状体回路。
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-08 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1470882
Ilaria Morella, Riccardo Brambilla, Yann Herault
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引用次数: 0
Exploring the biological basis of acupuncture treatment for traumatic brain injury: a review of evidence from animal models 探索针灸治疗脑外伤的生物学基础:动物模型证据综述
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-07 DOI: 10.3389/fncel.2024.1405782
Minmin Wu, Wenjing Song, Lili Teng, Jinting Li, Jiayu Liu, Hanwen Ma, Ge Zhang, Jiongliang Zhang, Qiuxin Chen
Traumatic brain injury (TBI) occurs when external physical forces impact the brain, potentially causing long-term issues such as post-traumatic stress disorders and cognitive and physical dysfunctions. The diverse nature of TBI pathology and treatment has led to a rapid acceleration in research on its biological mechanisms over the past decade. This surge presents challenges in assessing, managing, and predicting outcomes for TBI cases. Despite the development and testing of various therapeutic strategies aimed at mitigating neurological decline after TBI, a definitive cure for these conditions remains elusive. Recently, a growing focus has been on preclinical research investigating acupuncture as a potential treatment method for TBI sequelae. Acupuncture, being a cost-effective non-pharmacological therapy, has demonstrated promise in improving functional outcomes after brain injury. However, the precise mechanisms underlying the anticipated improvements induced by acupuncture remain poorly understood. In this study, we examined current evidence from animal studies regarding acupuncture’s efficacy in improving functional outcomes post-TBI. We also proposed potential biological mechanisms, such as glial cells (microglia astrocytes), autophagy, and apoptosis. This information will deepen our understanding of the underlying mechanisms through which acupuncture exerts its most beneficial effects post-TBI, assisting in forming new clinical strategies to maximize benefits for these patients.
创伤性脑损伤(TBI)发生于外部物理力量对大脑的冲击,可能导致创伤后应激障碍、认知和身体功能障碍等长期问题。创伤性脑损伤的病理和治疗具有多样性,因此在过去十年中,对其生物机制的研究迅速加速。这种激增给创伤性脑损伤病例的评估、管理和预后带来了挑战。尽管开发并测试了各种旨在缓解创伤后神经功能衰退的治疗策略,但这些病症的彻底治愈仍然遥遥无期。最近,针灸作为治疗创伤性脑损伤后遗症的一种潜在方法的临床前研究越来越受到关注。针灸作为一种经济有效的非药物疗法,在改善脑损伤后的功能预后方面已显示出希望。然而,人们对针灸改善脑损伤后遗症的确切机制仍知之甚少。在本研究中,我们考察了目前动物实验中有关针灸改善创伤后功能预后的证据。我们还提出了潜在的生物机制,如神经胶质细胞(小胶质细胞星形胶质细胞)、自噬和细胞凋亡。这些信息将加深我们对针灸在创伤后发挥最大疗效的潜在机制的理解,有助于形成新的临床策略,为这些患者带来最大益处。
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引用次数: 0
H7N7 viral infection elicits pronounced, sex-specific neuroinflammatory responses in vitro H7N7 病毒感染在体外引起明显的、有性别特异性的神经炎症反应
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-07 DOI: 10.3389/fncel.2024.1444876
Lea Gabele, Isabell Bochow, Nele Rieke, Christian Sieben, Kristin Michaelsen-Preusse, Shirin Hosseini, Martin Korte
Influenza A virus (IAV) infection can increase the risk of neuroinflammation, and subsequent neurodegenerative diseases. Certain IAV strains, such as avian H7N7 subtype, possess neurotropic properties, enabling them to directly invade the brain parenchyma and infect neurons and glia cells. Host sex significantly influences the severity of IAV infections. Studies indicate that females of the reproductive age exhibit stronger innate and adaptive immune responses to IAVs compared to males. This heightened immune response correlates with increased morbidity and mortality, and potential neuronal damage in females. Understanding the sex-specific neurotropism of IAV and associated mechanisms leading to adverse neurological outcomes is essential. Our study reveals that primary hippocampal cultures from female mice show heightened interferon-β and pro-inflammatory chemokine secretion following neurotropic IAV infection. We observed sex-specific differences in microglia activation: both sexes showed a transition into a hyper-ramified state, but only male-derived microglia exhibited an increase in amoeboid-shaped cells. These disparities extended to alterations in neuronal morphology. Neurons derived from female mice displayed increased spine density within 24 h post-infection, while no significant change was observed in male cultures. This aligns with sex-specific differences in microglial synaptic pruning. Data suggest that amoeboid-shaped microglia preferentially target postsynaptic terminals, potentially reducing neuronal hyperexcitability. Conversely, hyper-ramified microglia may focus on presynaptic terminals, potentially limiting viral spread. In conclusion, our findings underscore the utility of primary hippocampal cultures, incorporating microglia, as an effective model to study sex-specific, virus-induced effects on brain-resident cells.
感染甲型流感病毒(IAV)会增加神经发炎的风险,进而引发神经退行性疾病。某些 IAV 株系,如禽流感 H7N7 亚型,具有刺激神经的特性,可直接侵入脑实质,感染神经元和神经胶质细胞。宿主性别对 IAV 感染的严重程度有很大影响。研究表明,与男性相比,育龄女性对 IAV 表现出更强的先天性和适应性免疫反应。这种免疫反应的增强与女性发病率和死亡率的增加以及潜在的神经元损伤有关。了解 IAV 的性别特异性神经趋向性以及导致不良神经后果的相关机制至关重要。我们的研究发现,雌性小鼠的海马原代培养物在感染神经性 IAV 后,干扰素-β 和促炎趋化因子分泌增加。我们观察到了小胶质细胞活化的性别差异:雌雄小胶质细胞都表现出过度ramified状态,但只有雄性小胶质细胞表现出变形虫状细胞的增加。这些差异延伸到神经元形态的改变。来自雌性小鼠的神经元在感染后 24 小时内显示脊柱密度增加,而在雄性培养物中没有观察到明显变化。这与小胶质细胞突触修剪的性别差异一致。数据表明,变形虫状的小胶质细胞优先靶向突触后终端,从而可能降低神经元的过度兴奋性。相反,过度整型的小胶质细胞可能会集中于突触前终端,从而限制病毒的传播。总之,我们的研究结果表明,结合小胶质细胞的原代海马培养物是研究性特异性病毒对脑驻留细胞影响的有效模型。
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引用次数: 0
Neuroprotective and anti-inflammatory properties of proteins secreted by glial progenitor cells derived from human iPSCs 从人类 iPSCs 提取的神经胶质祖细胞分泌的蛋白质具有神经保护和抗炎特性
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-06 DOI: 10.3389/fncel.2024.1449063
Diana I. Salikhova, Margarita O. Shedenkova, Anastasya K. Sudina, Ekaterina V. Belousova, Irina A. Krasilnikova, Anastasya A. Nekrasova, Zlata A. Nefedova, Daniil A. Frolov, Timur Kh. Fatkhudinov, Andrey V. Makarov, Alexander M. Surin, Kirill V. Savostyanov, Dmitry V. Goldshtein, Zanda V. Bakaeva
Currently, stem cells technology is an effective tool in regenerative medicine. Cell therapy is based on the use of stem/progenitor cells to repair or replace damaged tissues or organs. This approach can be used to treat various diseases, such as cardiovascular, neurological diseases, and injuries of various origins. The mechanisms of cell therapy therapeutic action are based on the integration of the graft into the damaged tissue (replacement effect) and the ability of cells to secrete biologically active molecules such as cytokines, growth factors and other signaling molecules that promote regeneration (paracrine effect). However, cell transplantation has a number of limitations due to cell transportation complexity and immune rejection. A potentially more effective therapy is using only paracrine factors released by stem cells. Secreted factors can positively affect the damaged tissue: promote forming new blood vessels, stimulate cell proliferation, and reduce inflammation and apoptosis. In this work, we have studied the anti-inflammatory and neuroprotective effects of proteins with a molecular weight below 100 kDa secreted by glial progenitor cells obtained from human induced pluripotent stem cells. Proteins secreted by glial progenitor cells exerted anti-inflammatory effects in a primary glial culture model of LPS-induced inflammation by reducing nitric oxide (NO) production through inhibition of inducible NO synthase (iNOS). At the same time, added secreted proteins neutralized the effect of glutamate, increasing the number of viable neurons to control values. This effect is a result of decreased level of intracellular calcium, which, at elevated concentrations, triggers apoptotic death of neurons. In addition, secreted proteins reduce mitochondrial depolarization caused by glutamate excitotoxicity and help maintain higher NADH levels. This therapy can be successfully introduced into clinical practice after additional preclinical studies, increasing the effectiveness of rehabilitation of patients with neurological diseases.
目前,干细胞技术是再生医学的有效工具。细胞疗法是利用干细胞/祖细胞修复或替代受损组织或器官。这种方法可用于治疗各种疾病,如心血管疾病、神经系统疾病和各种原因造成的损伤。细胞疗法的治疗作用机制基于移植物与受损组织的整合(替代效应)以及细胞分泌生物活性分子(如细胞因子、生长因子和其他促进再生的信号分子)的能力(旁分泌效应)。然而,由于细胞运输的复杂性和免疫排斥反应,细胞移植有许多局限性。一种可能更有效的疗法是仅使用干细胞释放的旁分泌因子。分泌的因子可对受损组织产生积极影响:促进形成新血管、刺激细胞增殖、减少炎症和细胞凋亡。在这项工作中,我们研究了从人类诱导多能干细胞中获得的胶质祖细胞分泌的分子量低于100 kDa的蛋白质的抗炎和神经保护作用。神经胶质祖细胞分泌的蛋白质通过抑制诱导型一氧化氮合酶(iNOS)减少一氧化氮(NO)的产生,从而在LPS诱导的原代神经胶质培养模型中发挥抗炎作用。同时,添加的分泌蛋白还能中和谷氨酸的作用,将存活神经元的数量增加到控制值。这种效应是细胞内钙水平降低的结果,而高浓度的钙会引发神经元凋亡。此外,分泌蛋白还能降低谷氨酸兴奋毒性引起的线粒体去极化,并有助于维持较高的 NADH 水平。经过更多的临床前研究,这种疗法可以成功地应用于临床实践,提高神经系统疾病患者的康复效果。
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引用次数: 0
New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis 关于多发性硬化症中变性与自身免疫之间复杂相互作用的新观点
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-05 DOI: 10.3389/fncel.2024.1426231
Peter K. Stys, Shigeki Tsutsui, Arie R. Gafson, Bert A. ‘t Hart, Shibeshih Belachew, Jeroen J. G. Geurts
Multiple sclerosis (MS) is a frequently disabling neurological disorder characterized by symptoms, clinical signs and imaging abnormalities that typically fluctuate over time, affecting any level of the CNS. Prominent lymphocytic inflammation, many genetic susceptibility variants involving immune pathways, as well as potent responses of the neuroinflammatory component to immunomodulating drugs, have led to the natural conclusion that this disease is driven by a primary autoimmune process. In this Hypothesis and Theory article, we discuss emerging data that cast doubt on this assumption. After three decades of therapeutic experience, what has become clear is that potent immune modulators are highly effective at suppressing inflammatory relapses, yet exhibit very limited effects on the later progressive phase of MS. Moreover, neuropathological examination of MS tissue indicates that degeneration, CNS atrophy, and myelin loss are most prominent in the progressive stage, when lymphocytic inflammation paradoxically wanes. Finally, emerging clinical observations such as “progression independent of relapse activity” and “silent progression,” now thought to take hold very early in the course, together argue that an underlying “cytodegenerative” process, likely targeting the myelinating unit, may in fact represent the most proximal step in a complex pathophysiological cascade exacerbated by an autoimmune inflammatory overlay. Parallels are drawn with more traditional neurodegenerative disorders, where a progressive proteopathy with prion-like propagation of toxic misfolded species is now known to play a key role. A potentially pivotal contribution of the Epstein–Barr virus and B cells in this process is also discussed.
多发性硬化症(MS)是一种常见的致残性神经系统疾病,其症状、临床体征和影像学异常通常随时间而波动,影响中枢神经系统的任何层面。突出的淋巴细胞炎症、许多涉及免疫途径的遗传易感性变异以及神经炎症成分对免疫调节药物的强效反应,使人们自然而然地得出结论,这种疾病是由原发性自身免疫过程驱动的。在这篇 "假设与理论 "文章中,我们将讨论对这一假设产生怀疑的新数据。经过三十年的治疗经验,我们已经清楚地认识到,强效免疫调节剂在抑制炎症复发方面非常有效,但对多发性硬化症后期进展阶段的影响却非常有限。此外,多发性硬化症组织的神经病理学检查表明,变性、中枢神经系统萎缩和髓鞘脱失在进展期最为突出,而此时淋巴细胞炎症却在矛盾地减弱。最后,"进展与复发活动无关 "和 "无声进展 "等新出现的临床观察结果现在被认为在病程早期就已开始,这些观察结果共同表明,潜在的 "细胞变性 "过程(可能以髓鞘单元为目标)实际上可能是复杂病理生理级联中最接近的一步,而自身免疫性炎症叠加又加剧了这一过程。这与更多传统的神经退行性疾病相似,在这些疾病中,朊病毒样毒性错误折叠物种的渐进性蛋白病变起到了关键作用。此外,还讨论了 Epstein-Barr 病毒和 B 细胞在这一过程中可能起到的关键作用。
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引用次数: 0
Genome-wide sequencing identified extrachromosomal circular DNA as a transcription factor-binding motif of the senescence genes that govern replicative senescence in human mesenchymal stem cells 全基因组测序发现染色体外环状 DNA 是人类间充质干细胞中控制复制衰老的衰老基因的转录因子结合基序
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-02 DOI: 10.3389/fncel.2024.1421342
Wei Yang, Wei Ji, Boyu Liao, Zhongbo Li, Jian Wang, Haishu Lin, Jingbo Wang, Qian He
IntroductionMesenchymal stem cells (MSCs) have long been postulated as an important source cell in regenerative medicine. During subculture expansion, mesenchymal stem cell (MSC) senescence diminishes their multi-differentiation capabilities, leading to a loss of therapeutic potential. Up to date, the extrachromosomal circular DNAs (eccDNAs) have been demonstrated to be involved in senescence but the roles of eccDNAs during MSC.MethodsHere we explored eccDNA profiles in human bone marrow MSCs (BM-MSCs). EccDNA and mRNA was purified and sequenced, followed by quantification and functional annotation. Moreover, we mapped our datasets with the downloading enhancer and transcription factor-regulated genes to explore the potential role of eccDNAs.ResultsSequentially, gene annotation analysis revealed that the majority of eccDNA were mapped in the intron regions with limited BM-MSC enhancer overlaps. We discovered that these eccDNA motifs in senescent BMSCs acted as motifs for binding transcription factors (TFs) of senescence-related genes.DiscussionThese findings are highly significant for identifying biomarkers of senescence and therapeutic targets in mesenchymal stem cells (MSCs) for future clinical applications. The potential of eccDNA as a stable therapeutic target for senescence-related disorders warrants further investigation, particularly exploring chemically synthesized eccDNAs as transcription factor regulatory elements to reverse cellular senescence.
导言间充质干细胞(MSC)一直被认为是再生医学的重要源细胞。在亚培养扩增过程中,间充质干细胞(MSC)的衰老会削弱其多重分化能力,从而丧失治疗潜力。迄今为止,染色体外环状DNA(cccDNAs)已被证实参与衰老,但cccDNAs在间充质干细胞衰老过程中的作用尚待研究。我们对cccDNA和mRNA进行了纯化和测序,然后进行了定量和功能注释。此外,我们还将数据集与下载的增强子和转录因子调控基因进行了映射,以探索cccDNAs的潜在作用。结果基因注释分析表明,大多数cccDNA映射在内含子区域,与BM-MSC增强子重叠有限。我们发现,衰老的间充质干细胞中的这些cccDNA基团是衰老相关基因转录因子(TFs)的结合基团。eccDNA作为衰老相关疾病的稳定治疗靶点的潜力值得进一步研究,特别是探索化学合成的eccDNA作为转录因子调控元件来逆转细胞衰老。
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引用次数: 0
Revisiting a hypothesis: the neurovascular unit as a link between major depression and neurodegenerative disorders. 重新审视一个假设:神经血管单元是重度抑郁症和神经退行性疾病之间的联系。
IF 4.2 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-02 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1455606
Ravi Philip Rajkumar
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引用次数: 0
The role of SIRT3 in homeostasis and cellular health SIRT3 在平衡和细胞健康中的作用
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-08-02 DOI: 10.3389/fncel.2024.1434459
Dennison Trinh, Lina Al Halabi, Harsimar Brar, Marie Kametani, Joanne E. Nash
Mitochondria are responsible for maintaining cellular energy levels, and play a major role in regulating homeostasis, which ensures physiological function from the molecular to whole animal. Sirtuin 3 (SIRT3) is the major protein deacetylase of mitochondria. SIRT3 serves as a nutrient sensor; under conditions of mild metabolic stress, SIRT3 activity is increased. Within the mitochondria, SIRT3 regulates every complex of the electron transport chain, the tricarboxylic acid (TCA) and urea cycles, as well as the mitochondria membrane potential, and other free radical scavengers. This article reviews the role of SIRT3 in regulating homeostasis, and thus physiological function. We discuss the role of SIRT3 in regulating reactive oxygen species (ROS), ATP, immunological function and mitochondria dynamics.
线粒体负责维持细胞能量水平,并在调节体内平衡方面发挥重要作用,从而确保从分子到整个动物的生理功能。Sirtuin 3(SIRT3)是线粒体的主要蛋白质去乙酰化酶。SIRT3 是一种营养传感器;在轻微的代谢压力条件下,SIRT3 的活性会增加。在线粒体内,SIRT3 调节电子传递链、三羧酸(TCA)循环和尿素循环的每一个复合物,以及线粒体膜电位和其他自由基清除剂。本文回顾了 SIRT3 在调节体内平衡从而调节生理功能方面的作用。我们讨论了 SIRT3 在调节活性氧(ROS)、ATP、免疫功能和线粒体动力学方面的作用。
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引用次数: 0
Regional heterogeneity in the membrane properties of mouse striatal neurons 小鼠纹状体神经元膜特性的区域异质性
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-31 DOI: 10.3389/fncel.2024.1412897
Nao Chuhma, Stephen Rayport
The cytoarchitecture of the striatum is remarkably homogeneous, in contrast to the regional variation in striatal functions. Whether differences in the intrinsic membrane properties of striatal neurons contribute to regional heterogeneity has not been addressed systematically. We made recordings throughout the young adult mouse striatum under identical conditions, with synaptic input blocked, from four major striatal neuron types, namely, the two subtypes of spiny projection neurons (SPNs), cholinergic interneurons (ChIs), and fast-spiking GABAergic interneurons (FSIs), sampling at least 100 cells per cell type. Regional variation manifested across all cell types. All cell types in the nucleus accumbens (NAc) shell had higher input impedance and increased excitability. Cells in the NAc core were differentiated from the caudate-putamen (CPu) for both SPN subtypes by smaller action potentials and increased excitability. Similarity between the two SPN subtypes showed regional variation, differing more in the NAc than in the CPu. So, in the Str, both the intrinsic properties of interneurons and projection neurons are regionally heterogeneous, with the greatest difference between the NAc and CPu; greater excitability of NAc shell neurons may make the region more susceptible to activity-dependent plasticity.
纹状体的细胞结构非常均匀,这与纹状体功能的区域差异形成鲜明对比。纹状体神经元内在膜特性的差异是否导致了区域异质性,目前还没有系统的研究。我们在相同的条件下,在突触输入被阻断的情况下,对整个年轻成年小鼠纹状体的四种主要纹状体神经元类型进行了记录,这四种神经元类型是棘突投射神经元(SPN)的两种亚型、胆碱能中间神经元(ChIs)和快速尖峰 GABA 能中间神经元(FSIs),每种细胞类型至少取样 100 个细胞。所有细胞类型都存在区域差异。所有位于伏隔核(NAc)外壳的细胞类型都具有更高的输入阻抗和更高的兴奋性。对于两种 SPN 亚型而言,NAc 核心的细胞与尾状突起(CPu)的区别在于动作电位更小,兴奋性更高。两种 SPN 亚型之间的相似性表现出区域差异,在 NAc 的差异大于在 CPu 的差异。因此,在Str中,中间神经元和投射神经元的固有特性具有区域异质性,其中NAc和CPu之间的差异最大;NAc壳神经元的更高兴奋性可能使该区域更容易受到活动依赖性可塑性的影响。
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引用次数: 0
Neural ensembles: role of intrinsic excitability and its plasticity 神经集合:内在兴奋性的作用及其可塑性
IF 5.3 3区 医学 Q2 NEUROSCIENCES Pub Date : 2024-07-31 DOI: 10.3389/fncel.2024.1440588
Christian Hansel, Rafael Yuste
Synaptic connectivity defines groups of neurons that engage in correlated activity during specific functional tasks. These co-active groups of neurons form ensembles, the operational units involved in, for example, sensory perception, motor coordination and memory (then called an engram). Traditionally, ensemble formation has been thought to occur via strengthening of synaptic connections via long-term potentiation (LTP) as a plasticity mechanism. This synaptic theory of memory arises from the learning rules formulated by Hebb and is consistent with many experimental observations. Here, we propose, as an alternative, that the intrinsic excitability of neurons and its plasticity constitute a second, non-synaptic mechanism that could be important for the initial formation of ensembles. Indeed, enhanced neural excitability is widely observed in multiple brain areas subsequent to behavioral learning. In cortical structures and the amygdala, excitability changes are often reported as transient, even though they can last tens of minutes to a few days. Perhaps it is for this reason that they have been traditionally considered as modulatory, merely supporting ensemble formation by facilitating LTP induction, without further involvement in memory function (memory allocation hypothesis). We here suggest−based on two lines of evidence—that beyond modulating LTP allocation, enhanced excitability plays a more fundamental role in learning. First, enhanced excitability constitutes a signature of active ensembles and, due to it, subthreshold synaptic connections become suprathreshold in the absence of synaptic plasticity (iceberg model). Second, enhanced excitability promotes the propagation of dendritic potentials toward the soma and allows for enhanced coupling of EPSP amplitude (LTP) to the spike output (and thus ensemble participation). This permissive gate model describes a need for permanently increased excitability, which seems at odds with its traditional consideration as a short-lived mechanism. We propose that longer modifications in excitability are made possible by a low threshold for intrinsic plasticity induction, suggesting that excitability might be on/off-modulated at short intervals. Consistent with this, in cerebellar Purkinje cells, excitability lasts days to weeks, which shows that in some circuits the duration of the phenomenon is not a limiting factor in the first place. In our model, synaptic plasticity defines the information content received by neurons through the connectivity network that they are embedded in. However, the plasticity of cell-autonomous excitability could dynamically regulate the ensemble participation of individual neurons as well as the overall activity state of an ensemble.
突触连接定义了在特定功能任务中参与相关活动的神经元群。这些共同活动的神经元群形成了神经元集合,即参与感官知觉、运动协调和记忆等活动的操作单元(当时被称为 "映像")。传统上,人们认为神经元集合的形成是通过作为可塑性机制的长期电位(LTP)强化突触连接而实现的。这种突触记忆理论源于赫伯(Hebb)提出的学习规则,并与许多实验观察结果相一致。在这里,我们提出了另一种观点,即神经元的内在兴奋性及其可塑性构成了第二种非突触机制,可能对集合的初始形成非常重要。事实上,在行为学习之后的多个脑区都能广泛观察到神经兴奋性的增强。在皮层结构和杏仁核中,兴奋性变化通常被报告为短暂的,尽管它们可以持续几十分钟到几天。也许正是因为这个原因,它们一直被认为是调节性的,只是通过促进 LTP 的诱导来支持集合的形成,而没有进一步参与记忆功能(记忆分配假说)。我们在此基于两个证据提出,除了调节 LTP 分配外,兴奋性增强在学习中还扮演着更基本的角色。首先,增强的兴奋性是活跃集合的标志,由于它的存在,在没有突触可塑性的情况下,阈下突触连接会变成阈上突触连接(冰山模型)。其次,兴奋性的增强促进了树突电位向体部的传播,并使 EPSP 振幅(LTP)与尖峰输出(从而使集合参与)的耦合增强。这种 "允许门 "模型描述了一种永久性兴奋性增加的需要,这似乎与它作为一种短暂机制的传统观点相悖。我们提出,由于内在可塑性诱导的阈值较低,因此兴奋性的较长时间改变是可能的,这表明兴奋性可能在短时间内进行开/关调节。与此相一致的是,在小脑浦肯野细胞中,兴奋性可持续数天至数周,这表明在某些回路中,兴奋性持续时间首先并不是限制因素。在我们的模型中,突触可塑性通过神经元所处的连接网络定义了神经元接收的信息内容。然而,细胞自主兴奋性的可塑性可以动态调节单个神经元的集合参与以及集合的整体活动状态。
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Frontiers in Cellular Neuroscience
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