Neural Plasticity最新文献_第8页

Localization of Presynaptic Plasticity Mechanisms Enables Functional Independence of Synaptic and Ectopic Transmission in the Cerebellum. 突触前可塑性机制的定位使小脑突触和异位传递功能独立。

IF 3.1 4区医学

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-06-10 DOI: 10.1155/2015/602356

Katharine L Dobson, Tomas C Bellamy

{"title":"Localization of Presynaptic Plasticity Mechanisms Enables Functional Independence of Synaptic and Ectopic Transmission in the Cerebellum.","authors":"Katharine L Dobson, Tomas C Bellamy","doi":"10.1155/2015/602356","DOIUrl":"https://doi.org/10.1155/2015/602356","url":null,"abstract":"In the cerebellar molecular layer parallel fibre terminals release glutamate from both the active zone and from extrasynaptic \"ectopic\" sites. Ectopic release mediates transmission to the Bergmann glia that ensheathe the synapse, activating Ca(2+)-permeable AMPA receptors and glutamate transporters. Parallel fibre terminals exhibit several forms of presynaptic plasticity, including cAMP-dependent long-term potentiation and endocannabinoid-dependent long-term depression, but it is not known whether these presynaptic forms of long-term plasticity also influence ectopic transmission to Bergmann glia. Stimulation of parallel fibre inputs at 16 Hz evoked LTP of synaptic transmission, but LTD of ectopic transmission. Pharmacological activation of adenylyl cyclase by forskolin caused LTP at Purkinje neurons, but only transient potentiation at Bergmann glia, reinforcing the concept that ectopic sites lack the capacity to express sustained cAMP-dependent potentiation. Activation of mGluR1 caused depression of synaptic transmission via retrograde endocannabinoid signalling but had no significant effect at ectopic sites. In contrast, activation of NMDA receptors suppressed both synaptic and ectopic transmission. The results suggest that the signalling mechanisms for presynaptic LTP and retrograde depression by endocannabinoids are restricted to the active zone at parallel fibre synapses, allowing independent modulation of synaptic transmission to Purkinje neurons and ectopic transmission to Bergmann glia. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"602356"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/602356","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34283009","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}

引用次数: 3

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

Neural Plasticity 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

{"title":"Evolution of Apparent Diffusion Coefficient and Fractional Anisotropy in the Cerebrum of Asphyxiated Newborns Treated with Hypothermia over the First Month of Life.","authors":"Saskia Kwan, Elodie Boudes, Anouk Benseler, Guillaume Gilbert, Christine Saint-Martin, Michael Shevell, Pia Wintermark","doi":"10.1155/2015/653727","DOIUrl":"https://doi.org/10.1155/2015/653727","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"653727"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/653727","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33884578","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}

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

Neural Plasticity 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

{"title":"Anandamide, Acting via CB2 Receptors, Alleviates LPS-Induced Neuroinflammation in Rat Primary Microglial Cultures.","authors":"Natalia Malek, Katarzyna Popiolek-Barczyk, Joanna Mika, Barbara Przewlocka, Katarzyna Starowicz","doi":"10.1155/2015/130639","DOIUrl":"https://doi.org/10.1155/2015/130639","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"130639"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/130639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33937937","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}

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

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-07-22 DOI: 10.1155/2015/358263

Ian A Clark, Bryce Vissel

{"title":"A Neurologist's Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in Disease.","authors":"Ian A Clark, Bryce Vissel","doi":"10.1155/2015/358263","DOIUrl":"https://doi.org/10.1155/2015/358263","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"358263"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/358263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33944909","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}

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

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-07-26 DOI: 10.1155/2015/135342

Stefano Morara, Anna Maria Colangelo, Luciano Provini

{"title":"Microglia-Induced Maladaptive Plasticity Can Be Modulated by Neuropeptides In Vivo.","authors":"Stefano Morara, Anna Maria Colangelo, Luciano Provini","doi":"10.1155/2015/135342","DOIUrl":"10.1155/2015/135342","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"135342"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33988629","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}

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

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-06-25 DOI: 10.1155/2015/753179

Hiroshi Ueno, Shunsuke Suemitsu, Yosuke Matsumoto, Motoi Okamoto

{"title":"Sensory Deprivation during Early Postnatal Period Alters the Density of Interneurons in the Mouse Prefrontal Cortex.","authors":"Hiroshi Ueno, Shunsuke Suemitsu, Yosuke Matsumoto, Motoi Okamoto","doi":"10.1155/2015/753179","DOIUrl":"https://doi.org/10.1155/2015/753179","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"753179"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/753179","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33893036","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}

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

Neural Plasticity 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

{"title":"Effect of Prolonged Moderate Exercise on the Changes of Nonneuronal Cells in Early Myocardial Infarction.","authors":"Barbara Rinaldi, Francesca Guida, Anna Furiano, Maria Donniacuo, Livio Luongo, Giulia Gritti, Konrad Urbanek, Giovanni Messina, Sabatino Maione, Francesco Rossi, Vito de Novellis","doi":"10.1155/2015/265967","DOIUrl":"https://doi.org/10.1155/2015/265967","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"265967"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/265967","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33982591","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}

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

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-08-04 DOI: 10.1155/2015/902802

Jessica N Holland, Adam T Schmidt

{"title":"Static and Dynamic Factors Promoting Resilience following Traumatic Brain Injury: A Brief Review.","authors":"Jessica N Holland, Adam T Schmidt","doi":"10.1155/2015/902802","DOIUrl":"10.1155/2015/902802","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"902802"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4539485/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33982805","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}

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

Neural Plasticity Pub Date : 2015-01-01 Epub Date: 2015-08-26 DOI: 10.1155/2015/687175

Emiliano Merlo, Pedro Bekinschtein, Sietse Jonkman, Jorge H Medina

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

Neural Plasticity 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

{"title":"Neural Plastic Effects of Cognitive Training on Aging Brain.","authors":"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","doi":"10.1155/2015/535618","DOIUrl":"https://doi.org/10.1155/2015/535618","url":null,"abstract":"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. ","PeriodicalId":51299,"journal":{"name":"Neural Plasticity","volume":"2015 ","pages":"535618"},"PeriodicalIF":3.1,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2015/535618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34045481","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}

引用次数: 47