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Evolution of Apparent Diffusion Coefficient and Fractional Anisotropy in the Cerebrum of Asphyxiated Newborns Treated with Hypothermia over the First Month of Life. 在出生后第一个月接受低温治疗的窒息新生儿大脑中表观扩散系数和分数各向异性的演变。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-07-02 DOI: 10.1155/2015/653727
Saskia Kwan, Elodie Boudes, Anouk Benseler, Guillaume Gilbert, Christine Saint-Martin, Michael Shevell, Pia Wintermark

The objective of this study was to assess the evolution of diffusion-weighted imaging (DWI) and diffusion-tensor imaging (DTI) over the first month of life in asphyxiated newborns treated with hypothermia and to compare it with that of healthy newborns. Asphyxiated newborns treated with hypothermia were enrolled prospectively; and the presence and extent of brain injury were scored on each MRI. Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) values were measured in the basal ganglia, in the white matter and in the cortical grey matter. Sixty-one asphyxiated newborns treated with hypothermia had a total of 126 ADC and FA maps. Asphyxiated newborns developing brain injury eventually had significantly decreased ADC values on days 2-3 of life and decreased FA values around day 10 and 1 month of life compared with those not developing brain injury. Despite hypothermia treatment, asphyxiated newborns may develop brain injury that still can be detected with advanced neuroimaging techniques such as DWI and DTI as early as days 2-3 of life. A study of ADC and FA values over time may aid in the understanding of how brain injury develops in these newborns despite hypothermia treatment.

本研究的目的是评估经低温治疗的窒息新生儿在生命第一个月内弥散加权成像(DWI)和弥散张量成像(DTI)的演变,并将其与健康新生儿进行比较。采用低温治疗的窒息新生儿被纳入前瞻性研究;并在每次MRI上对脑损伤的存在和程度进行评分。测定基底节、白质和皮质灰质的表观扩散系数(ADC)和分数各向异性(FA)值。61例经低温治疗的窒息新生儿共126张ADC和FA图。与未发生脑损伤的新生儿相比,发生脑损伤的窒息新生儿在出生后2-3天的ADC值和10天和1个月的FA值最终显著降低。尽管进行了低温治疗,但窒息的新生儿仍可能出现脑损伤,这种损伤可以在出生后2-3天通过DWI和DTI等先进的神经成像技术检测到。随着时间的推移,ADC和FA值的研究可能有助于理解这些新生儿在接受低温治疗后脑损伤是如何发展的。
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引用次数: 8
Anandamide, Acting via CB2 Receptors, Alleviates LPS-Induced Neuroinflammation in Rat Primary Microglial Cultures. 阿南达胺通过CB2受体减轻lps诱导的大鼠初级小胶质细胞炎症
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-05-18 DOI: 10.1155/2015/130639
Natalia Malek, Katarzyna Popiolek-Barczyk, Joanna Mika, Barbara Przewlocka, Katarzyna Starowicz

Microglial activation is a polarized process divided into potentially neuroprotective phenotype M2 and neurotoxic phenotype M1, predominant during chronic neuroinflammation. Endocannabinoid system provides an attractive target to control the balance between microglial phenotypes. Anandamide as an immune modulator in the central nervous system acts via not only cannabinoid receptors (CB1 and CB2) but also other targets (e.g., GPR18/GPR55). We studied the effect of anandamide on lipopolysaccharide-induced changes in rat primary microglial cultures. Microglial activation was assessed based on nitric oxide (NO) production. Analysis of mRNA was conducted for M1 and M2 phenotype markers possibly affected by the treatment. Our results showed that lipopolysaccharide-induced NO release in microglia was significantly attenuated, with concomitant downregulation of M1 phenotypic markers, after pretreatment with anandamide. This effect was not sensitive to CB1 or GPR18/GPR55 antagonism. Administration of CB2 antagonist partially abolished the effects of anandamide on microglia. Interestingly, administration of a GPR18/GPR55 antagonist by itself suppressed NO release. In summary, we showed that the endocannabinoid system plays a crucial role in the management of neuroinflammation by dampening the activation of an M1 phenotype. This effect was primarily controlled by the CB2 receptor, although functional cross talk with GPR18/GPR55 may occur.

小胶质细胞激活是一个极化过程,分为潜在的神经保护表型M2和神经毒性表型M1,主要在慢性神经炎症期间。内源性大麻素系统为控制小胶质细胞表型之间的平衡提供了一个有吸引力的靶点。Anandamide作为中枢神经系统中的免疫调节剂,不仅通过大麻素受体(CB1和CB2)起作用,还通过其他靶点(例如GPR18/GPR55)起作用。我们研究了阿南德胺对脂多糖诱导大鼠原代小胶质细胞变化的影响。根据一氧化氮(NO)的产生评估小胶质细胞的激活。对可能受处理影响的M1和M2表型标记进行mRNA分析。我们的研究结果表明,经过anandamide预处理后,脂多糖诱导的小胶质细胞NO释放明显减弱,同时M1表型标记下调。该效应对CB1或GPR18/GPR55拮抗剂不敏感。给药CB2拮抗剂部分消除了阿南胺对小胶质细胞的作用。有趣的是,单独给药GPR18/GPR55拮抗剂可抑制NO释放。总之,我们发现内源性大麻素系统通过抑制M1表型的激活在神经炎症的管理中起着至关重要的作用。这种作用主要由CB2受体控制,尽管与GPR18/GPR55可能发生功能性串扰。
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引用次数: 87
A Neurologist's Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in Disease. 神经科医生的TNF生物学指南和治疗性去除疾病中过量TNF的原则。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-07-22 DOI: 10.1155/2015/358263
Ian A Clark, Bryce Vissel

Tumor necrosis factor (TNF) is an ancient and widespread cytokine required in small amounts for much physiological function. Higher concentrations are central to innate immunity, but if unchecked this cytokine orchestrates much chronic and acute disease, both infectious and noninfectious. While being a major proinflammatory cytokine, it also controls homeostasis and plasticity in physiological circumstances. For the last decade or so these principles have been shown to apply to the central nervous system as well as the rest of the body. Nevertheless, whereas this approach has been a major success in treating noncerebral disease, its investigation and potential widespread adoption in chronic neurological conditions has inexplicably stalled since the first open trial almost a decade ago. While neuroscience is closely involved with this approach, clinical neurology appears to be reticent in engaging with what it offers patients. Unfortunately, the basic biology of TNF and its relevance to disease is largely outside the traditions of neurology. The purpose of this review is to facilitate lowering communication barriers between the traditional anatomically based medical specialties through recognition of shared disease mechanisms and thus advance the prospects of a large group of patients with neurodegenerative conditions for whom at present little can be done.

肿瘤坏死因子(TNF)是一种古老而广泛存在的细胞因子,在许多生理功能中需要少量的细胞因子。较高的浓度对先天免疫至关重要,但如果不加以控制,这种细胞因子会导致许多慢性和急性疾病,包括传染性和非传染性疾病。作为一种主要的促炎细胞因子,它还控制着生理环境中的内稳态和可塑性。在过去十年左右的时间里,这些原理已经被证明适用于中枢神经系统以及身体的其他部分。然而,尽管这种方法在治疗非脑疾病方面取得了重大成功,但自近10年前首次公开试验以来,它在慢性神经系统疾病方面的研究和潜在的广泛应用却莫名其妙地停滞不前。虽然神经科学与这种方法密切相关,但临床神经病学似乎对它为患者提供的服务持保留态度。不幸的是,TNF的基本生物学及其与疾病的相关性在很大程度上超出了神经病学的传统。本综述的目的是通过认识共同的疾病机制来降低传统解剖学医学专业之间的交流障碍,从而提高目前几乎无法做到的一大群神经退行性疾病患者的前景。
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引用次数: 23
Microglia-Induced Maladaptive Plasticity Can Be Modulated by Neuropeptides In Vivo. 体内神经肽可调节小胶质细胞诱导的不良可塑性
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-07-26 DOI: 10.1155/2015/135342
Stefano Morara, Anna Maria Colangelo, Luciano Provini

Microglia-induced maladaptive plasticity is being recognized as a major cause of deleterious self-sustaining pathological processes that occur in neurodegenerative and neuroinflammatory diseases. Microglia, the primary homeostatic guardian of the central nervous system, exert critical functions both during development, in neural circuit reshaping, and during adult life, in the brain physiological and pathological surveillance. This delicate critical role can be disrupted by neural, but also peripheral, noxious stimuli that can prime microglia to become overreactive to a second noxious stimulus or worsen underlying pathological processes. Among regulators of microglia, neuropeptides can play a major role. Their receptors are widely expressed in microglial cells and neuropeptide challenge can potently influence microglial activity in vitro. More relevantly, this regulator activity has been assessed also in vivo, in experimental models of brain diseases. Neuropeptide action in the central nervous system has been associated with beneficial effects in neurodegenerative and neuroinflammatory pathological experimental models. This review describes some of the mechanisms of the microglia maladaptive plasticity in vivo and how neuropeptide activity can represent a useful therapeutical target in a variety of human brain pathologies.

小胶质细胞诱导的不适应可塑性被认为是神经退行性疾病和神经炎症性疾病中有害的自我持续病理过程的主要原因。小胶质细胞是中枢神经系统的主要稳态守护者,在发育过程中和成年后分别在神经回路重塑和大脑生理与病理监控方面发挥着关键作用。这种微妙的关键作用会受到神经和外周有害刺激的破坏,这些刺激会使小胶质细胞对第二次有害刺激产生过度反应,或使潜在的病理过程恶化。在小胶质细胞的调节因子中,神经肽可以发挥重要作用。它们的受体在小胶质细胞中广泛表达,神经肽挑战可在体外对小胶质细胞的活动产生有效影响。更重要的是,在脑部疾病的实验模型中,这种调节活性也在体内得到了评估。神经肽在中枢神经系统中的作用与神经退行性病变和神经炎症病理实验模型中的有益效应有关。本综述介绍了体内小胶质细胞适应性不良可塑性的一些机制,以及神经肽活性如何成为各种人类脑部疾病的有用治疗靶点。
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引用次数: 0
Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex. 产后早期感觉剥夺改变小鼠前额叶皮层中间神经元密度。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-06-25 DOI: 10.1155/2015/753179
Hiroshi Ueno, Shunsuke Suemitsu, Yosuke Matsumoto, Motoi Okamoto

Early loss of one sensory system can cause improved function of other sensory systems. However, both the time course and neuronal mechanism of cross-modal plasticity remain elusive. Recent study using functional MRI in humans suggests a role of the prefrontal cortex (PFC) in cross-modal plasticity. Since this phenomenon is assumed to be associated with altered GABAergic inhibition in the PFC, we have tested the hypothesis that early postnatal sensory deprivation causes the changes of inhibitory neuronal circuit in different regions of the PFC of the mice. We determined the effects of sensory deprivation from birth to postnatal day 28 (P28) or P58 on the density of parvalbumin (PV), calbindin (CB), and calretinin (CR) neurons in the prelimbic, infralimbic, and dorsal anterior cingulate cortices. The density of PV and CB neurons was significantly increased in layer 5/6 (L5/6). Moreover, the density of CR neurons was higher in L2/3 in sensory deprived mice compared to intact mice. These changes were more prominent at P56 than at P28. These results suggest that long-term sensory deprivation causes the changes of intracortical inhibitory networks in the PFC and the changes of inhibitory networks in the PFC may contribute to cross-modal plasticity.

早期一个感觉系统的丧失会导致其他感觉系统功能的改善。然而,跨模态可塑性的时间过程和神经元机制尚不清楚。最近在人类中使用功能性MRI的研究表明前额皮质(PFC)在跨模态可塑性中的作用。由于这一现象被认为与PFC中GABAergic抑制的改变有关,我们已经测试了出生后早期感觉剥夺导致小鼠PFC不同区域抑制性神经元回路的变化的假设。我们测定了从出生到出生后第28天(P28)或第58天感觉剥夺对边缘前、边缘下和背前扣带皮层中小白蛋白(PV)、钙结合蛋白(CB)和钙化蛋白(CR)神经元密度的影响。第5/6层(L5/6) PV和CB神经元密度显著增加。感觉剥夺小鼠L2/3区CR神经元密度明显高于正常小鼠。这些变化在P56位点比P28位点更为明显。这些结果表明,长期感觉剥夺导致PFC皮层内抑制网络的变化,PFC抑制网络的变化可能有助于跨模态可塑性。
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引用次数: 9
Effect of Prolonged Moderate Exercise on the Changes of Nonneuronal Cells in Early Myocardial Infarction. 长期适度运动对早期心肌梗死非神经元细胞变化的影响。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-07-22 DOI: 10.1155/2015/265967
Barbara Rinaldi, Francesca Guida, Anna Furiano, Maria Donniacuo, Livio Luongo, Giulia Gritti, Konrad Urbanek, Giovanni Messina, Sabatino Maione, Francesco Rossi, Vito de Novellis

Myocardial infarction (MI) is one of the leading causes of death in developed countries and it is characterized by several associated symptomatologies and poor quality of life. Recent data showed a possible interaction between infarction and brain inflammation and activity. Previous studies have demonstrated the beneficial effect of exercise training on deterioration in cardiac function after MI. In this study we analyzed in sedentary and trained rats the microglia and astrocytes 48 hours after MI in PVN, thalamus, prefrontal cortex, and hippocampus through immunofluorescence approach. We found significant changes in specific microglia phenotypes in the brain areas analyzed together with astrocytes activation. Prolonged exercise normalized these morphological changes of microglia and astrocytes in the prefrontal cortex, hippocampus, and thalamus but not in the PVN. Our data suggest that there is an early brain reaction to myocardial infarction induction, involving nonneuronal cells, that is attenuated by the prolonged exercise.

心肌梗死(MI)是发达国家的主要死亡原因之一,其特点是几种相关症状和生活质量差。最近的数据显示,梗死与大脑炎症和活动之间可能存在相互作用。先前的研究已经证明运动训练对心肌梗死后心功能恶化有有益作用。在本研究中,我们通过免疫荧光法分析了久坐和训练大鼠心肌梗死后48小时内PVN、丘脑、前额叶皮层和海马的小胶质细胞和星形胶质细胞。我们发现,在星形胶质细胞激活的大脑区域中,特定的小胶质细胞表型发生了显著变化。长时间的运动使前额皮质、海马和丘脑的小胶质细胞和星形胶质细胞的形态变化正常化,但PVN却没有。我们的数据表明,大脑对心肌梗死诱导有早期反应,涉及非神经元细胞,这种反应因长时间运动而减弱。
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引用次数: 47
Static and Dynamic Factors Promoting Resilience following Traumatic Brain Injury: A Brief Review. 促进创伤性脑损伤后恢复能力的静态和动态因素:简要回顾。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-08-04 DOI: 10.1155/2015/902802
Jessica N Holland, Adam T Schmidt

Traumatic brain injury (TBI) is the greatest contributing cause of death and disability among children and young adults in the United States. The current paper briefly summarizes contemporary literature on factors that can improve outcomes (i.e., promote resilience) for children and adults following TBI. For the purpose of this paper, the authors divided these factors into static or unmodifiable factors (i.e., age, sex, intellectual abilities/education, and preinjury psychiatric history) and dynamic or modifiable factors (i.e., socioeconomic status, family functioning/social support, nutrition, and exercise). Drawing on human and animal studies, the research reviewed indicated that these various factors can improve outcomes in multiple domains of functioning (e.g., cognition, emotion regulation, health and wellness, behavior, etc.) following a TBI. However, many of these factors have not been studied across populations, have been limited to preclinical investigations, have been limited in their scope or follow-up, or have not involved a thorough evaluation of outcomes. Thus, although promising, continued research is vital in the area of factors promoting resilience following TBI in children and adults.

创伤性脑损伤(TBI)是造成美国儿童和青少年死亡和残疾的最大原因。本文简要总结了有关可改善儿童和成人创伤性脑损伤后的结果(即促进恢复能力)的因素的当代文献。在本文中,作者将这些因素分为静态或不可改变的因素(即年龄、性别、智力/教育程度和受伤前精神病史)和动态或可改变的因素(即社会经济状况、家庭功能/社会支持、营养和锻炼)。通过对人类和动物的研究,所审查的研究表明,这些不同的因素可以改善创伤性脑损伤后多个功能领域(如认知、情绪调节、健康和保健、行为等)的结果。然而,其中许多因素尚未在不同人群中进行研究,仅限于临床前调查,研究范围或后续研究有限,或未对结果进行全面评估。因此,尽管前景广阔,但在促进儿童和成人创伤后复原力的因素方面,继续开展研究至关重要。
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引用次数: 0
Molecular Mechanisms of Memory Consolidation, Reconsolidation, and Persistence. 记忆巩固、再巩固和持久的分子机制。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-08-26 DOI: 10.1155/2015/687175
Emiliano Merlo, Pedro Bekinschtein, Sietse Jonkman, Jorge H Medina
Fil: Merlo, Emiliano. University of Cambridge; Reino Unido. Consejo Nacional de Investigaciones Cientificas y Tecnicas; Argentina
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引用次数: 13
Neural Plastic Effects of Cognitive Training on Aging Brain. 认知训练对衰老大脑的神经可塑性影响。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-08-31 DOI: 10.1155/2015/535618
Natalie T Y Leung, Helena M K Tam, Leung W Chu, Timothy C Y Kwok, Felix Chan, Linda C W Lam, Jean Woo, Tatia M C Lee

Increasing research has evidenced that our brain retains a capacity to change in response to experience until late adulthood. This implies that cognitive training can possibly ameliorate age-associated cognitive decline by inducing training-specific neural plastic changes at both neural and behavioral levels. This longitudinal study examined the behavioral effects of a systematic thirteen-week cognitive training program on attention and working memory of older adults who were at risk of cognitive decline. These older adults were randomly assigned to the Cognitive Training Group (n = 109) and the Active Control Group (n = 100). Findings clearly indicated that training induced improvement in auditory and visual-spatial attention and working memory. The training effect was specific to the experience provided because no significant difference in verbal and visual-spatial memory between the two groups was observed. This pattern of findings is consistent with the prediction and the principle of experience-dependent neuroplasticity. Findings of our study provided further support to the notion that the neural plastic potential continues until older age. The baseline cognitive status did not correlate with pre- versus posttraining changes to any cognitive variables studied, suggesting that the initial cognitive status may not limit the neuroplastic potential of the brain at an old age.

越来越多的研究证明,直到成年后期,我们的大脑仍有能力根据经验做出改变。这意味着认知训练可能通过在神经和行为水平上诱导训练特异性的神经可塑性变化来改善与年龄相关的认知衰退。这项纵向研究考察了一个为期13周的系统性认知训练项目对有认知能力下降风险的老年人的注意力和工作记忆的行为影响。这些老年人被随机分配到认知训练组(n = 109)和积极对照组(n = 100)。研究结果清楚地表明,训练诱导了听觉、视觉空间注意力和工作记忆的改善。训练效果是特定于所提供的经验的,因为两组之间在言语和视觉空间记忆方面没有观察到显著差异。这种发现模式与经验依赖神经可塑性的预测和原理是一致的。我们的研究结果进一步支持了神经可塑性潜能会持续到老年的观点。基线认知状态与研究的任何认知变量的训练前后变化无关,这表明初始认知状态可能不会限制老年大脑的神经可塑性潜力。
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引用次数: 47
Hippocampal Infusion of Zeta Inhibitory Peptide Impairs Recent, but Not Remote, Recognition Memory in Rats. 海马注入Zeta抑制肽损害大鼠近期而非远端识别记忆。
IF 3.1 4区 医学 Q2 NEUROSCIENCES Pub Date : 2015-01-01 Epub Date: 2015-08-24 DOI: 10.1155/2015/847136
Jena B Hales, Amber C Ocampo, Nicola J Broadbent, Robert E Clark

Spatial memory in rodents can be erased following the infusion of zeta inhibitory peptide (ZIP) into the dorsal hippocampus via indwelling guide cannulas. It is believed that ZIP impairs spatial memory by reversing established late-phase long-term potentiation (LTP). However, it is unclear whether other forms of hippocampus-dependent memory, such as recognition memory, are also supported by hippocampal LTP. In the current study, we tested recognition memory in rats following hippocampal ZIP infusion. In order to combat the limited targeting of infusions via cannula, we implemented a stereotaxic approach for infusing ZIP throughout the dorsal, intermediate, and ventral hippocampus. Rats infused with ZIP 3-7 days after training on the novel object recognition task exhibited impaired object recognition memory compared to control rats (those infused with aCSF). In contrast, rats infused with ZIP 1 month after training performed similar to control rats. The ability to form new memories after ZIP infusions remained intact. We suggest that enhanced recognition memory for recent events is supported by hippocampal LTP, which can be reversed by hippocampal ZIP infusion.

zeta抑制肽(ZIP)通过留置引导管注入海马背侧后,可以消除啮齿类动物的空间记忆。人们认为,ZIP通过逆转已建立的后期长期增强(LTP)而损害空间记忆。然而,海马体LTP是否也支持其他形式的海马体依赖记忆,如识别记忆,目前尚不清楚。在本研究中,我们测试了海马ZIP输注后大鼠的识别记忆。为了克服通过插管输注的局限性,我们采用立体定向方法在整个海马背侧、中间和腹侧输注ZIP。在新目标识别任务训练后3-7天注射ZIP的大鼠与注射aCSF的对照大鼠相比,物体识别记忆受损。相比之下,训练后1个月注射ZIP的大鼠表现与对照组相似。注射ZIP后形成新记忆的能力保持不变。我们认为海马LTP支持对近期事件的增强识别记忆,而海马ZIP输注可以逆转这一过程。
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引用次数: 8
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