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[PMID]:28542213
[Au] Autor:Gross C; Ellison B; Buchman AS; Terasawa E; VanderHorst VG
[Ad] Endereço:Department of Neurology, Division of Movement Disorders, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.
[Ti] Título:A novel approach for assigning levels to monkey and human lumbosacral spinal cord based on ventral horn morphology.
[So] Source:PLoS One;12(5):e0177243, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proper identification of spinal cord levels is crucial for clinical-pathological and imaging studies in humans, but can be a challenge given technical limitations. We have previously demonstrated in non-primate models that the contours of the spinal ventral horn are determined by the position of motoneuron pools. These positions are preserved within and among individuals and can be used to identify lumbosacral spinal levels. Here we tested the hypothesis that this approach can be extended to identify monkey and human spinal levels. In 7 rhesus monkeys, we retrogradely labeled motoneuron pools that represent rostral, middle and caudal landmarks of the lumbosacral enlargement. We then aligned the lumbosacral enlargements among animals using absolute length, segmental level or a relative scale based upon rostral and caudal landmarks. Inter-animal matching of labeled motoneurons across the lumbosacral enlargement was most precise when using internal landmarks. We then reconstructed 3 human lumbosacral spinal cords, and aligned these based upon homologous internal landmarks. Changes in shape of the ventral horn were consistent among human subjects using this relative scale, despite marked differences in absolute length or age. These data suggest that the relative position of spinal motoneuron pools is conserved across species, including primates. Therefore, in clinical-pathological or imaging studies in humans, one can assign spinal cord levels to even single sections by matching ventral horn shape to standardized series.
[Mh] Termos MeSH primário: Células do Corno Anterior/citologia
Região Lombossacral/anatomia & histologia
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Animais
Gatos
Feminino
Fixadores
Formaldeído
Seres Humanos
Macaca mulatta
Masculino
Meia-Idade
Técnicas de Rastreamento Neuroanatômico
Marcadores do Trato Nervoso
Especificidade da Espécie
Fixação de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fixatives); 0 (Neuronal Tract-Tracers); 1HG84L3525 (Formaldehyde)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177243


  2 / 1028 MEDLINE  
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[PMID]:28048973
[Au] Autor:Kassa RM; Bonafede R; Boschi F; Bentivoglio M; Mariotti R
[Ad] Endereço:Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Verona, Italy.
[Ti] Título:Effect of physical exercise and anabolic steroid treatment on spinal motoneurons and surrounding glia of wild-type and ALS mice.
[So] Source:Brain Res;1657:269-278, 2017 Feb 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Motoneuron degeneration is the hallmark of amyotrophic lateral sclerosis (ALS). The cause and predisposing factors for sporadic ALS are still unknown. Exposure to a specific environmental risk factors in subjects with a susceptibility genotype may increase the risk of the disease. The role of physical activity and the use of anabolic steroids are still debated in epidemiological studies on patients and murine models of ALS. To assess at the cellular level the role (beneficial or detrimental) of physical exercise and the use of anabolic steroid, we here investigated, in SOD1(G93A) (mSOD1) mice and wild-type littermates, changes in the ventral horn after regular exercise, treatment with the anabolic androgenic steroid 19-nortestosterone (nandrolone), and their combination, compared with matched control sedentary mice. The experiments were pursued for several weeks until symptom onset in mSOD1 mice. Lumbar motoneurons, astrocytes and microglia were analyzed. In wild-type mice, cytological alterations of motoneurons were observed especially after nandrolone treatment. The following main findings were observed in treated mSOD1 mice versus untreated ones: i) nandrolone treatment markedly enhanced motoneuron loss; this detrimental effect was reverted by the combination with exercise, resulting in increased motoneuron survival; ii) astrocytic activation was most marked after nandrolone treatment when motoneuron damage was most severe; iii) microglia activation was most marked after physical exercise when motoneuron damage was less severe. The results indicate a vulnerability of mSOD1 motoneurons to nandrolone treatment, a potential neuroprotective effect of physical exercise, and a modulation by glial cells in the ALS murine model in the examined paradigms.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/terapia
Anabolizantes/farmacologia
Células do Corno Anterior/fisiologia
Terapia por Exercício
Nandrolona/farmacologia
Neuroglia/fisiologia
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/patologia
Esclerose Amiotrófica Lateral/fisiopatologia
Anabolizantes/toxicidade
Animais
Células do Corno Anterior/efeitos dos fármacos
Células do Corno Anterior/patologia
Peso Corporal
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Colina O-Acetiltransferase/metabolismo
Modelos Animais de Doenças
Vértebras Lombares
Masculino
Camundongos Transgênicos
Nandrolona/toxicidade
Neuroglia/efeitos dos fármacos
Neuroglia/patologia
Distribuição Aleatória
Corrida/fisiologia
Estilo de Vida Sedentário
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anabolic Agents); 6PG9VR430D (Nandrolone); EC 2.3.1.6 (Choline O-Acetyltransferase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE


  3 / 1028 MEDLINE  
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[PMID]:28003344
[Au] Autor:Garg N; Park SB; Vucic S; Yiannikas C; Spies J; Howells J; Huynh W; Matamala JM; Krishnan AV; Pollard JD; Cornblath DR; Reilly MM; Kiernan MC
[Ad] Endereço:Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.
[Ti] Título:Differentiating lower motor neuron syndromes.
[So] Source:J Neurol Neurosurg Psychiatry;88(6):474-483, 2017 Jun.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lower motor neuron (LMN) syndromes typically present with muscle wasting and weakness and may arise from pathology affecting the distal motor nerve up to the level of the anterior horn cell. A variety of hereditary causes are recognised, including spinal muscular atrophy, distal hereditary motor neuropathy and LMN variants of familial motor neuron disease. Recent genetic advances have resulted in the identification of a variety of disease-causing mutations. Immune-mediated disorders, including multifocal motor neuropathy and variants of chronic inflammatory demyelinating polyneuropathy, account for a proportion of LMN presentations and are important to recognise, as effective treatments are available. The present review will outline the spectrum of LMN syndromes that may develop in adulthood and provide a framework for the clinician assessing a patient presenting with predominantly LMN features.
[Mh] Termos MeSH primário: Doença dos Neurônios Motores/diagnóstico
[Mh] Termos MeSH secundário: Células do Corno Anterior/patologia
Autoanticorpos/análise
Análise Mutacional de DNA
Diagnóstico Diferencial
Seres Humanos
Doença dos Neurônios Motores/genética
Doença dos Neurônios Motores/patologia
Neurônios Motores/patologia
Atrofia Muscular Espinal/diagnóstico
Atrofia Muscular Espinal/genética
Atrofia Muscular Espinal/patologia
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/diagnóstico
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/genética
Polirradiculoneuropatia Desmielinizante Inflamatória Crônica/patologia
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2016-313526


  4 / 1028 MEDLINE  
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[PMID]:27600517
[Au] Autor:Henderson RD; McCombe PA
[Ad] Endereço:Department of Neurology, Royal Brisbane & Women's Hospital and University of Queensland Centre for Clinical Research, Herston, Brisbane, 4006, Australia. robert.henderson@health.qld.gov.au.
[Ti] Título:Assessment of Motor Units in Neuromuscular Disease.
[So] Source:Neurotherapeutics;14(1):69-77, 2017 Jan.
[Is] ISSN:1878-7479
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The motor unit comprises the anterior horn cell, its axon, and the muscle fibers that it innervates. Although the true number of motor units is unknown, the number of motor units appears to vary greatly between different muscles and between different individuals. Assessment of the number and function of motor units is needed in diseases of the anterior horn cell and other motor nerve disorders. Amyotrophic lateral sclerosis is the most important disease of anterior horn cells. The need for an effective biomarker for assessing disease progression and for use in clinical trials in amyotrophic lateral sclerosis has stimulated the study of methods to measure the number of motor units. Since 1970 a number of different methods, including the incremental, F-wave, multipoint, and statistical methods, have been developed but none has achieved widespread applicability. Two methods (MUNIX and the multipoint incremental method) are in current use across multiple centres and are discussed in detail in this review, together with other recently published methods. Imaging with magnetic resonance and ultrasound is increasingly being applied to this area. Motor unit number estimates have also been applied to other neuromuscular diseases such as spinal muscular atrophy, compression neuropathies, and prior poliomyelitis. The need for an objective measure for the assessment of motor units remains tantalizingly close but unfulfilled in 2016.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/diagnóstico
Esclerose Amiotrófica Lateral/fisiopatologia
Células do Corno Anterior/fisiologia
Músculo Esquelético/fisiopatologia
Doenças Neuromusculares/diagnóstico
Doenças Neuromusculares/fisiopatologia
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/diagnóstico por imagem
Biomarcadores
Progressão da Doença
Estimulação Elétrica
Eletromiografia
Seres Humanos
Imagem por Ressonância Magnética
Condução Nervosa
Doenças Neuromusculares/diagnóstico por imagem
Ultrassonografia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160908
[St] Status:MEDLINE
[do] DOI:10.1007/s13311-016-0473-z


  5 / 1028 MEDLINE  
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[PMID]:27825148
[Au] Autor:Smith AS; Passey SL; Martin NR; Player DJ; Mudera V; Greensmith L; Lewis MP
[Ti] Título:Creating Interactions between Tissue-Engineered Skeletal Muscle and the Peripheral Nervous System.
[So] Source:Cells Tissues Organs;202(3-4):143-158, 2016.
[Is] ISSN:1422-6421
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Effective models of mammalian tissues must allow and encourage physiologically (mimetic) correct interactions between co-cultured cell types in order to produce culture microenvironments as similar as possible to those that would normally occur in vivo. In the case of skeletal muscle, the development of such a culture model, integrating multiple relevant cell types within a biomimetic scaffold, would be of significant benefit for investigations into the development, functional performance, and pathophysiology of skeletal muscle tissue. Although some work has been published regarding the behaviour of in vitro muscle models co-cultured with organotypic slices of CNS tissue or with stem cell-derived neurospheres, little investigation has so far been made regarding the potential to maintain isolated motor neurons within a 3D biomimetic skeletal muscle culture platform. Here, we review the current state of the art for engineering neuromuscular contacts in vitro and provide original data detailing the development of a 3D collagen-based model for the co-culture of primary muscle cells and motor neurons. The devised culture system promotes increased myoblast differentiation, forming arrays of parallel, aligned myotubes on which areas of nerve-muscle contact can be detected by immunostaining for pre- and post-synaptic proteins. Quantitative RT-PCR results indicate that motor neuron presence has a positive effect on myotube maturation, suggesting neural incorporation influences muscle development and maturation in vitro. The importance of this work is discussed in relation to other published neuromuscular co-culture platforms along with possible future directions for the field.
[Mh] Termos MeSH primário: Músculo Esquelético/fisiologia
Sistema Nervoso Periférico/fisiologia
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Animais
Células do Corno Anterior/citologia
Células do Corno Anterior/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Técnicas de Cocultura
Meios de Cultura/farmacologia
Matriz Extracelular/efeitos dos fármacos
Matriz Extracelular/metabolismo
Géis
Regulação da Expressão Gênica/efeitos dos fármacos
Camundongos
Neurônios Motores/citologia
Neurônios Motores/efeitos dos fármacos
Músculo Esquelético/citologia
Músculo Esquelético/efeitos dos fármacos
Neuritos/efeitos dos fármacos
Neuritos/metabolismo
Ratos Sprague-Dawley
Sinapses/efeitos dos fármacos
Sinapses/metabolismo
Tecidos Suporte/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Culture Media); 0 (Gels)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE


  6 / 1028 MEDLINE  
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[PMID]:27588715
[Au] Autor:Wang S; Liang Z; Gong Y; Yin Y; Wang K; He Q; Wang Z; Bai J
[Ad] Endereço:Institute of Photonics and Photon-Technology, Northwest University, Xi'an, Shaanxi, China. Electronic address: wsnwuphy@163.com.
[Ti] Título:Confocal raman microspectral imaging of ex vivo human spinal cord tissue.
[So] Source:J Photochem Photobiol B;163:177-84, 2016 Oct.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Confocal Raman microspectral imaging (CRMI) provides a versatile tool to illustrate the biochemical nature and structure of biological tissue without introducing any external labels. In this work, a precise correlation was established between the biochemical profile and histological architecture of ex vivo human spinal cord tissue by using CRMI with 633nm excitation. After precisely linking the spectral features to the chemical constituents, much information about the molecular composition of both gray and white matter were revealed. Two-dimensional Raman images were generated by integrating the intensities of the characteristic Raman bands in the area of the intermediate column and ventral horn. K-mean cluster analysis was further applied to visualize the underlying morphological basis of spinal cord tissue by chemical component types and their distribution pattern. Lipid-rich white matter could be visually distinguished from gray matter considering a CH2 bending/scissoring band at 1445cm(-1) and an amide III band at 1250cm(-1). Meanwhile, the formation and distribution pattern of perineuronal nets (PNNs) in the scanning area was validated by the integration of saccharides (617cm(-1)) and amide III bands. Moreover, the heme profile indicated a higher degree of vascularization in gray matter. All of the results obtained testified to the possibility that gray matter could be more susceptible to spinal cord injury (SCI) because of capillary network distribution and glycosaminoglycans (GAGs) aggregation. These findings are important for interpreting the morphological specificity of human spinal cord tissue, and also for studying the molecular basis of SCI.
[Mh] Termos MeSH primário: Imagem Molecular/métodos
Análise Espectral Raman
Medula Espinal/citologia
[Mh] Termos MeSH secundário: Células do Corno Anterior/citologia
Seres Humanos
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170317
[Lr] Data última revisão:
170317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160903
[St] Status:MEDLINE


  7 / 1028 MEDLINE  
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[PMID]:27343829
[Au] Autor:Ohashi M; Hirano T; Watanabe K; Shoji H; Ohashi N; Baba H; Endo N; Kohno T
[Ad] Endereço:Division of Orthopedic Surgery, Department of Regenerative and Transplant Medicine, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi Dori, Chuo-Ku, Niigata City 951-8510, Japan.
[Ti] Título:Hydrogen peroxide modulates neuronal excitability and membrane properties in ventral horn neurons of the rat spinal cord.
[So] Source:Neuroscience;331:206-20, 2016 Sep 07.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hydrogen peroxide (H2O2), a reactive oxygen species, is an important signaling molecule for synaptic and neuronal activity in the central nervous system; it is produced excessively in brain ischemia and spinal cord injury. Although H2O2-mediated modulations of synaptic transmission have been reported in ventral horn (VH) neurons of the rat spinal cord, the effects of H2O2 on neuronal excitability and membrane properties remain poorly understood. Accordingly, the present study investigated such effects using a whole-cell patch-clamp technique. The bath-application of H2O2 decreased neuronal excitability accompanied by decreased input resistance, firing frequency, and action potential amplitude and by increased rheobase. These H2O2-mediated changes were induced by activation of extrasynaptic, but not synaptic, GABAA receptors. Indeed, GABAergic tonic currents were enhanced by H2O2. On the other hand, the amplitude of medium and slow afterhyperpolarization (mAHP and sAHP), which plays important roles in controlling neuronal excitability and is mediated by small-conductance calcium-activated potassium (SK) channels, was significantly decreased by H2O2. When extrasynaptic GABAA receptors were completely blocked, these decreases of mAHP and sAHP persisted, and H2O2 increased excitability, suggesting that H2O2 per se might have the potential to increase neuronal excitability via decreased SK channel conductance. These findings indicate that activating extrasynaptic GABAA receptors or SK channels may attenuate acute neuronal damage caused by H2O2-induced hyperexcitability and therefore represent a novel therapeutic target for the prevention and treatment of H2O2-induced motor neuron disorders.
[Mh] Termos MeSH primário: Células do Corno Anterior/fisiologia
Peróxido de Hidrogênio/metabolismo
Potenciais da Membrana/fisiologia
[Mh] Termos MeSH secundário: Animais
Células do Corno Anterior/efeitos dos fármacos
Bicuculina/farmacologia
Relação Dose-Resposta a Droga
Peróxido de Hidrogênio/farmacologia
Potenciais da Membrana/efeitos dos fármacos
Inibição Neural/efeitos dos fármacos
Inibição Neural/fisiologia
Neurotransmissores/farmacologia
Técnicas de Patch-Clamp
Ratos Wistar
Receptores de GABA-A/metabolismo
Receptores da Glicina/metabolismo
Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo
Estricnina/farmacologia
Sinapses/efeitos dos fármacos
Sinapses/metabolismo
Técnicas de Cultura de Tecidos
Ácido gama-Aminobutírico/metabolismo
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (Receptors, GABA-A); 0 (Receptors, Glycine); 0 (Small-Conductance Calcium-Activated Potassium Channels); 56-12-2 (gamma-Aminobutyric Acid); BBX060AN9V (Hydrogen Peroxide); H9Y79VD43J (Strychnine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160626
[St] Status:MEDLINE


  8 / 1028 MEDLINE  
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[PMID]:27256400
[Au] Autor:Umahara T; Uchihara T; Shibata N; Nakamura A; Hanyu H
[Ad] Endereço:Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan; Laboratory of Structural Neuropathology, Tokyo Metropolitan Institute of Medical Science, 2-1-9 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan. Electronic address: takahiko@tokyo-me
[Ti] Título:14-3-3 eta isoform colocalizes TDP-43 on the coarse granules in the anterior horn cells of patients with sporadic amyotrophic lateral sclerosis.
[So] Source:Brain Res;1646:132-138, 2016 Sep 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The immunolocalization of the 14-3-3 eta isoform in the anterior horn cells (AHCs) of patients with sporadic amyotrophic lateral sclerosis (ALS) and controls was examined. Compared with the immunolocalization of other 14-3-3 isoforms, the immunolocalization of the 14-3-3 eta isoform was either synaptic at the periphery of AHCs, spindle-shaped in neurites, or granular in the cytoplasm. By double labeling with phosphorylated (p-)TDP-43, the transactivation response DNA binding protein of 43kDa (TDP-43) demonstrated frequent colocalization of the 14-3-3 eta isoform in granular structures (90%) and spindle-shaped structures (85.4%), but not in p-TDP-43-positive round inclusions. It is speculated that the 14-3-3 eta isoform is associated with not only a synaptic pathology of ALS but also TDP-positive small lesions in the cytoplasm and neurites. The absence of eta-like immunoreactivity in p-TDP-43-positive large inclusions suggests the restricted relevance of the 14-3-3 eta isoform during ALS pathogenesis to some phases of the p-TDP pathology.
[Mh] Termos MeSH primário: Proteínas 14-3-3/metabolismo
Esclerose Amiotrófica Lateral/metabolismo
Células do Corno Anterior/metabolismo
Proteínas de Ligação a DNA/metabolismo
[Mh] Termos MeSH secundário: Idoso
Grânulos Citoplasmáticos/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Neuritos/metabolismo
Isoformas de Proteínas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (14-3-3 Proteins); 0 (DNA-Binding Proteins); 0 (Protein Isoforms); 0 (TDP-43 protein, human); 0 (YWHAH protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170806
[Lr] Data última revisão:
170806
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160604
[St] Status:MEDLINE


  9 / 1028 MEDLINE  
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[PMID]:27028103
[Au] Autor:Cirillo G; Colangelo AM; De Luca C; Savarese L; Barillari MR; Alberghina L; Papa M
[Ad] Endereço:Laboratory of Neuronal Networks, Department. of Mental and Physical Health and Preventive Medicine, Second University of Naples, 80138 Naples, Italy.
[Ti] Título:Modulation of Matrix Metalloproteinases Activity in the Ventral Horn of the Spinal Cord Re-stores Neuroglial Synaptic Homeostasis and Neurotrophic Support following Peripheral Nerve Injury.
[So] Source:PLoS One;11(3):e0152750, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Modulation of extracellular matrix (ECM) remodeling after peripheral nerve injury (PNI) could represent a valid therapeutic strategy to prevent maladaptive synaptic plasticity in central nervous system (CNS). Inhibition of matrix metalloproteinases (MMPs) and maintaining a neurotrophic support could represent two approaches to prevent or reduce the maladaptive plastic changes in the ventral horn of spinal cord following PNI. The purpose of our study was to analyze changes in the ventral horn produced by gliopathy determined by the suffering of motor neurons following spared nerve injury (SNI) of the sciatic nerve and how the intrathecal (i.t.) administration of GM6001 (a MMPs inhibitor) or the NGF mimetic peptide BB14 modulate these events. Immunohistochemical analysis of spinal cord sections revealed that motor neuron disease following SNI was associated with increased microglial (Iba1) and astrocytic (GFAP) response in the ventral horn of the spinal cord, indicative of reactive gliosis. These changes were paralleled by decreased glial aminoacid transporters (glutamate GLT1 and glycine GlyT1), increased levels of the neuronal glutamate transporter EAAC1, and a net increase of the Glutamate/GABA ratio, as measured by HPLC analysis. These molecular changes correlated to a significant reduction of mature NGF levels in the ventral horn. Continuous i.t. infusion of both GM6001 and BB14 reduced reactive astrogliosis, recovered the expression of neuronal and glial transporters, lowering the Glutamate/GABA ratio. Inhibition of MMPs by GM6001 significantly increased mature NGF levels, but it was absolutely ineffective in modifying the reactivity of microglia cells. Therefore, MMPs inhibition, although supplies neurotrophic support to ECM components and restores neuro-glial transporters expression, differently modulates astrocytic and microglial response after PNI.
[Mh] Termos MeSH primário: Células do Corno Anterior/enzimologia
Astrócitos/enzimologia
Gelatinases/metabolismo
Microglia/enzimologia
Traumatismos dos Nervos Periféricos/enzimologia
Nervo Isquiático/enzimologia
Nervo Isquiático/lesões
Medula Espinal/enzimologia
Sinapses/enzimologia
[Mh] Termos MeSH secundário: Animais
Células do Corno Anterior/patologia
Astrócitos/patologia
Dipeptídeos/farmacologia
Gelatinases/antagonistas & inibidores
Proteínas de Transporte de Glutamato da Membrana Plasmática/metabolismo
Ácido Glutâmico/metabolismo
Proteínas da Membrana Plasmática de Transporte de Glicina/metabolismo
Masculino
Microglia/patologia
Traumatismos dos Nervos Periféricos/patologia
Ratos
Ratos Sprague-Dawley
Nervo Isquiático/patologia
Medula Espinal/patologia
Sinapses/patologia
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dipeptides); 0 (Glutamate Plasma Membrane Transport Proteins); 0 (Glycine Plasma Membrane Transport Proteins); 0 (N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide); 0 (Slc6a9 protein, rat); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); EC 3.4.24.- (Gelatinases)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0152750


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Fotocópia
Mendez-Otero, Rosalia
PubMed Central Texto completo
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[PMID]:26979533
[Au] Autor:Gubert F; Decotelli AB; Bonacossa-Pereira I; Figueiredo FR; Zaverucha-do-Valle C; Tovar-Moll F; Hoffmann L; Urmenyi TP; Santiago MF; Mendez-Otero R
[Ad] Endereço:Instituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Sala G2-028, Universidade Federal do Rio de Janeiro, Cidade Universitária, RJ 21941-902, Rio de Janeiro, Brazil. fegubert@biof.ufrj.br.
[Ti] Título:Intraspinal bone-marrow cell therapy at pre- and symptomatic phases in a mouse model of amyotrophic lateral sclerosis.
[So] Source:Stem Cell Res Ther;7:41, 2016 Mar 15.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a progressive neurological disease that selectively affects the motor neurons. The details of the mechanisms of selective motor-neuron death remain unknown and no effective therapy has been developed. We investigated the therapy with bone-marrow mononuclear cells (BMMC) in a mouse model of ALS (SOD1(G93A) mice). METHODS: We injected 10(6) BMMC into the lumbar portion of the spinal cord of SOD1(G93A) mice in presymptomatic (9 weeks old) and symptomatic (14 weeks old) phases. In each condition, we analyzed the progression of disease and the lifespan of the animals. RESULTS: We observed a mild transitory delay in the disease progression in the animals injected with BMMC in the presymptomatic phase. However, we observed no increase in the lifespan. When we injected BMMC in the symptomatic phase, we observed no difference in the animals' lifespan or in the disease progression. Immunohistochemistry for NeuN showed a decrease in the number of motor neurons during the course of the disease, and this decrease was not affected by either treatment. Using different strategies to track the BMMC, we noted that few cells remained in the spinal cord after transplantation. This observation could explain why the BMMC therapy had only a transitory effect. CONCLUSION: This is the first report of intraspinal BMMC therapy in a mouse model of ALS. We conclude this cellular therapy has only a mild transitory effect when performed in the presymptomatic phase of the disease.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/terapia
Doenças Assintomáticas/terapia
Transplante de Medula Óssea
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/fisiopatologia
Animais
Células do Corno Anterior/fisiologia
Movimento Celular
Sobrevivência Celular
Rastreamento de Células
Feminino
Injeções Espinhais
Região Lombossacral/patologia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microglia/fisiologia
Atividade Motora
Mutação de Sentido Incorreto
Recuperação de Função Fisiológica
Superóxido Dismutase/genética
Superóxido Dismutase-1
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.15.1.1 (Sod1 protein, mouse); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (Superoxide Dismutase-1)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160317
[St] Status:MEDLINE
[do] DOI:10.1186/s13287-016-0293-4



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