Base de dados : MEDLINE
Pesquisa : E05.017.449 [Categoria DeCS]
Referências encontradas : 1313 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 132 ir para página                         

  1 / 1313 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28456003
[Au] Autor:Röhr D; Halfter H; Schulz JB; Young P; Gess B
[Ad] Endereço:Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Muenster, Muenster, Germany.
[Ti] Título:Sodium-dependent Vitamin C transporter 2 deficiency impairs myelination and remyelination after injury: Roles of collagen and demethylation.
[So] Source:Glia;65(7):1186-1200, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral nerve myelination involves rapid production of tightly bound lipid layers requiring cholesterol biosynthesis and myelin protein expression, but also a collagen-containing extracellular matrix providing mechanical stability. In previous studies, we showed a function of ascorbic acid in peripheral nerve myelination and extracellular matrix formation in adult mice. Here, we sought the mechanism of action of ascorbic acid in peripheral nerve myelination using different paradigms of myelination in vivo and in vitro. We found impaired myelination and reduced collagen expression in Sodium-dependent Vitamin C Transporter 2 heterozygous mice (SVCT2 ) during peripheral nerve development and after peripheral nerve injury. In dorsal root ganglion (DRG) explant cultures, hypo-myelination could be rescued by precoating with different collagen types. The activity of the ascorbic acid-dependent demethylating Ten-eleven-translocation (Tet) enzymes was reduced in ascorbic acid deprived and SVCT2 DRG cultures. Further, in ascorbic acid-deprived DRG cultures, methylation of a CpG island in the collagen alpha1 (IV) and alpha2 (IV) bidirectional promoter region was increased compared to wild-type and ascorbic acid treated controls. Taken together, these results provide further evidence for the function of ascorbic acid in myelination and extracellular matrix formation in peripheral nerves and suggest a putative molecular mechanism of ascorbic acid function in Tet-dependent demethylation of collagen promoters.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Desmetilação
Traumatismos dos Nervos Periféricos/genética
Traumatismos dos Nervos Periféricos/fisiopatologia
Remielinização/genética
Transportadores de Sódio Acoplados à Vitamina C/deficiência
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Células Cultivadas
Colágeno/genética
Modelos Animais de Doenças
Feminino
Transtornos Neurológicos da Marcha/etiologia
Gânglios Espinais/citologia
Masculino
Camundongos
Camundongos Transgênicos
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
RNA Mensageiro/metabolismo
Teste de Desempenho do Rota-Rod
Células Receptoras Sensoriais/metabolismo
Células Receptoras Sensoriais/patologia
Transportadores de Sódio Acoplados à Vitamina C/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Slc23a2 protein, mouse); 0 (Sodium-Coupled Vitamin C Transporters); 9007-34-5 (Collagen); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23152


  2 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29244816
[Au] Autor:Avila-Martin G; Mata-Roig M; Galán-Arriero I; Taylor JS; Busquets X; Escribá PV
[Ad] Endereço:Hospital Nacional de Parapléjicos, Toledo, Spain.
[Ti] Título:Treatment with albumin-hydroxyoleic acid complex restores sensorimotor function in rats with spinal cord injury: Efficacy and gene expression regulation.
[So] Source:PLoS One;12(12):e0189151, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sensorimotor dysfunction following incomplete spinal cord injury (SCI) is often characterized by paralysis, spasticity and pain. Previously, we showed that intrathecal (i.t.) administration of the albumin-oleic acid (A-OA) complex in rats with SCI produced partial improvement of these symptoms and that oral 2-hydroxyoleic acid (HOA, a non-hydrolyzable OA analogue), was efficacious in the modulation and treatment of nociception and pain-related anxiety, respectively. Here we observed that intrathecal treatment with the complex albumin-HOA (A-HOA) every 3 days following T9 spinal contusion injury improved locomotor function assessed with the Rotarod and inhibited TA noxious reflex activity in Wistar rats. To investigate the mechanism of action of A-HOA, microarray analysis was carried out in the spinal cord lesion area. Representative genes involved in pain and neuroregeneration were selected to validate the changes observed in the microarray analysis by quantitative real-time RT-PCR. Comparison of the expression between healthy rats, SCI rats, and SCI treated with A-HOA rats revealed relevant changes in the expression of genes associated with neuronal morphogenesis and growth, neuronal survival, pain and inflammation. Thus, treatment with A-HOA not only induced a significant overexpression of growth and differentiation factor 10 (GDF10), tenascin C (TNC), aspirin (ASPN) and sushi-repeat-containing X-linked 2 (SRPX2), but also a significant reduction in the expression of prostaglandin E synthase (PTGES) and phospholipases A1 and A2 (PLA1/2). Currently, SCI has very important unmet clinical needs. A-HOA downregulated genes involved with inflammation and upregulated genes involved in neuronal growth, and may serve to promote recovery of function after experimental SCI.
[Mh] Termos MeSH primário: Albuminas/farmacologia
Ácidos Oleicos/farmacologia
Dor/prevenção & controle
Paralisia/tratamento farmacológico
Recuperação de Função Fisiológica/efeitos dos fármacos
Traumatismos da Medula Espinal/tratamento farmacológico
[Mh] Termos MeSH secundário: Albuminas/química
Animais
Esquema de Medicação
Proteínas da Matriz Extracelular/agonistas
Proteínas da Matriz Extracelular/genética
Proteínas da Matriz Extracelular/metabolismo
Regulação da Expressão Gênica
Fator 10 de Diferenciação de Crescimento/agonistas
Fator 10 de Diferenciação de Crescimento/genética
Fator 10 de Diferenciação de Crescimento/metabolismo
Injeções Espinhais
Locomoção/efeitos dos fármacos
Locomoção/fisiologia
Masculino
Proteínas do Tecido Nervoso/agonistas
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Nociceptividade/efeitos dos fármacos
Ácidos Oleicos/química
Dor/genética
Dor/metabolismo
Dor/patologia
Paralisia/genética
Paralisia/metabolismo
Paralisia/patologia
Fosfolipases/antagonistas & inibidores
Fosfolipases/genética
Fosfolipases/metabolismo
Prostaglandina-E Sintases/antagonistas & inibidores
Prostaglandina-E Sintases/genética
Prostaglandina-E Sintases/metabolismo
Ratos
Ratos Wistar
Recuperação de Função Fisiológica/fisiologia
Teste de Desempenho do Rota-Rod
Medula Espinal/efeitos dos fármacos
Medula Espinal/metabolismo
Medula Espinal/patologia
Traumatismos da Medula Espinal/genética
Traumatismos da Medula Espinal/metabolismo
Traumatismos da Medula Espinal/patologia
Tenascina/agonistas
Tenascina/genética
Tenascina/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-hydroxyoleic acid); 0 (Albumins); 0 (Extracellular Matrix Proteins); 0 (Gdf10 protein, rat); 0 (Growth Differentiation Factor 10); 0 (Nerve Tissue Proteins); 0 (Oleic Acids); 0 (Tenascin); 0 (asporin protein, rat); EC 3.1.- (Phospholipases); EC 5.3.99.3 (Prostaglandin-E Synthases); EC 5.3.99.3 (Ptges protein, rat)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189151


  3 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28867578
[Au] Autor:Rostami F; Javan M; Moghimi A; Haddad-Mashadrizeh A; Fereidoni M
[Ad] Endereço:Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran.
[Ti] Título:Streptozotocin-induced hippocampal astrogliosis and insulin signaling malfunction as experimental scales for subclinical sporadic Alzheimer model.
[So] Source:Life Sci;188:172-185, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Insulin signaling malfunction has recently been suggested as a preliminary event involved in the etiology of Sporadic Alzheimer's disease (SAD). In order to develop insulin resistance-related SAD model, rats were treated with streptozotocin, intracerebroventricularly (icv-STZ). Nevertheless, given the lack of knowledge regarding sub-clinical stages of SAD, the current challenging issue is establishing a practical pre-clinical SAD model. Despite some proposed mechanisms, such as insulin malfunction, neuroinflammation, and gliosis, icv-STZ mechanism of action is not fully understood yet and Streptozotocin-induced rat model of Alzheimer has still major shortcomings. MAIN METHODS: Using three STZ doses (0.5, 1, and 3mg/kg) and three testing time (short-term, medium-term and long-term), we sought the best dose of STZ in order to mimic the characteristic feature of sAD in rats. So, we conducted a series of fifteen-week follow-up cognitive and non-cognitive studies. Besides, IR, tau and ChAT mRNA levels were measured, along with histological analysis of astrocyte, dark neuron numbers, and pyramidal layer thickness, in order to compare the effects of different doses of icv-STZ. KEY FINDINGS: STZ 3mg/kg caused cognitive and insulin signaling disturbance from the very first testing-time. STZ1-injected animals, however, showed an augmented hippocampal astrocyte numbers in a short time; they, also, were diagnosed with disturbed insulin signaling in medium-term post icv-STZ-injection. Moreover, behavioral, molecular and histological impairments induced by 0.5mg/kg icv-STZ were slowly progressing in comparison to high doses of STZ. SIGNIFICANCE: STZ1 and 0.5mg/kg-treated animals are, respectively, suggested as a suitable experimental model of MCI, and sub-clinical stage.
[Mh] Termos MeSH primário: Doença de Alzheimer/diagnóstico
Gliose/patologia
Hipocampo/patologia
Resistência à Insulina
Insulina/metabolismo
Sintomas Prodrômicos
Estreptozocina/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Astrócitos/patologia
Colina O-Acetiltransferase/biossíntese
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Comportamento Exploratório/efeitos dos fármacos
Gliose/induzido quimicamente
Infusões Intraventriculares
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Neurônios/patologia
Ratos
Receptor de Insulina/biossíntese
Recognição (Psicologia)/efeitos dos fármacos
Teste de Desempenho do Rota-Rod
Estreptozocina/administração & dosagem
Fatores de Tempo
Proteínas tau/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (tau Proteins); 5W494URQ81 (Streptozocin); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 2.7.10.1 (Receptor, Insulin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


  4 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28753236
[Au] Autor:Sauer RS; Kirchner J; Yang S; Hu L; Leinders M; Sommer C; Brack A; Rittner HL
[Ad] Endereço:Department of Anesthesiology and Critical Care, University Hospital of Würzburg, Würzburg, Germany.
[Ti] Título:Blood-spinal cord barrier breakdown and pericyte deficiency in peripheral neuropathy.
[So] Source:Ann N Y Acad Sci;1405(1):71-88, 2017 Oct.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The blood-spinal cord barrier (BSCB) prevents leakage of molecules, such as pronociceptive mediators, into the spinal cord, but its role in the pathophysiology of neuropathic pain is not completely understood. Rats with chronic constriction injury (CCI) develop mechanical allodynia, thermal hypersensitivity, and reduced motor performance (Rota-Rod test) compared with sham-injured mice-similar to mice with spared nerve injury (SNI). The BSCB becomes permeable for small and large tracers 1 day after nerve ligation. Messenger RNA (mRNA) expression of tight junction proteins (TJPs) occludin, claudin-1, claudin-5, claudin-19, tricellulin, and ZO-1 significantly declines 7-14 days after CCI or SNI. ZO-1 and occludin are reduced in the cell membrane. In capillaries isolated from the spinal cord, immunoreactivity of claudin-5 and ZO-1 is fainter. In parallel, the number of platelet-derived growth factor receptor ß (PDGF-ß) and CD13 pericytes in the spinal cord drops. Reduced levels of cytosolic transcription factors like ß-catenin, but not SMAD4 and SLUG, could account for reduced TJP mRNA. In summary, neuropathy-induced allodynia/hypersensitivity is accompanied by a loss of pericytes in the spinal cord and a leaky BSCB. A better understanding of these pathways and mechanisms in neuropathic pain might foster the design of novel treatments to maintain spinal cord homeostasis.
[Mh] Termos MeSH primário: Pericitos/metabolismo
Doenças do Sistema Nervoso Periférico/metabolismo
Medula Espinal/metabolismo
Proteínas de Junções Íntimas/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Destreza Motora/fisiologia
Pericitos/patologia
Doenças do Sistema Nervoso Periférico/patologia
Permeabilidade
Ratos
Ratos Wistar
Teste de Desempenho do Rota-Rod
Proteína Smad4/metabolismo
Fatores de Transcrição da Família Snail/metabolismo
Medula Espinal/patologia
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Smad4 Protein); 0 (Snai2 protein, rat); 0 (Snail Family Transcription Factors); 0 (Tight Junction Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13436


  5 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28405024
[Au] Autor:Scoles DR; Meera P; Schneider MD; Paul S; Dansithong W; Figueroa KP; Hung G; Rigo F; Bennett CF; Otis TS; Pulst SM
[Ad] Endereço:Department of Neurology, University of Utah, 175 North Medical Drive East, 5th Floor, Salt Lake City, Utah 84132, USA.
[Ti] Título:Antisense oligonucleotide therapy for spinocerebellar ataxia type 2.
[So] Source:Nature;544(7650):362-366, 2017 04 20.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:There are no disease-modifying treatments for adult human neurodegenerative diseases. Here we test RNA-targeted therapies in two mouse models of spinocerebellar ataxia type 2 (SCA2), an autosomal dominant polyglutamine disease. Both models recreate the progressive adult-onset dysfunction and degeneration of a neuronal network that are seen in patients, including decreased firing frequency of cerebellar Purkinje cells and a decline in motor function. We developed a potential therapy directed at the ATXN2 gene by screening 152 antisense oligonucleotides (ASOs). The most promising oligonucleotide, ASO7, downregulated ATXN2 mRNA and protein, which resulted in delayed onset of the SCA2 phenotype. After delivery by intracerebroventricular injection to ATXN2-Q127 mice, ASO7 localized to Purkinje cells, reduced cerebellar ATXN2 expression below 75% for more than 10 weeks without microglial activation, and reduced the levels of cerebellar ATXN2. Treatment of symptomatic mice with ASO7 improved motor function compared to saline-treated mice. ASO7 had a similar effect in the BAC-Q72 SCA2 mouse model, and in both mouse models it normalized protein levels of several SCA2-related proteins expressed in Purkinje cells, including Rgs8, Pcp2, Pcp4, Homer3, Cep76 and Fam107b. Notably, the firing frequency of Purkinje cells returned to normal even when treatment was initiated more than 12 weeks after the onset of the motor phenotype in BAC-Q72 mice. These findings support ASOs as a promising approach for treating some human neurodegenerative diseases.
[Mh] Termos MeSH primário: Oligonucleotídeos Antissenso/uso terapêutico
Ataxias Espinocerebelares/genética
Ataxias Espinocerebelares/terapia
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Ataxina-2/deficiência
Ataxina-2/genética
Ataxina-2/metabolismo
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Movimento
Fenótipo
Células de Purkinje/metabolismo
Células de Purkinje/patologia
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Teste de Desempenho do Rota-Rod
Ataxias Espinocerebelares/patologia
Ataxias Espinocerebelares/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATXN2 protein, human); 0 (Ataxin-2); 0 (Atxn2 protein, mouse); 0 (Oligonucleotides, Antisense); 0 (RNA, Messenger)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE
[do] DOI:10.1038/nature22044


  6 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28400118
[Au] Autor:Liang LP; Huang J; Fulton R; Pearson-Smith JN; Day BJ; Patel M
[Ad] Endereço:Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO, United States.
[Ti] Título:Pre-clinical therapeutic development of a series of metalloporphyrins for Parkinson's disease.
[So] Source:Toxicol Appl Pharmacol;326:34-42, 2017 Jul 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactive oxygen species are a well-defined therapeutic target for Parkinson's disease (PD) and pharmacological agents that catalytically scavenge reactive species are promising neuroprotective strategies for treatment. Metalloporphyrins are synthetic catalytic antioxidants that mimic the body's own antioxidant enzymes i.e. superoxide dismutases and catalase. The goal of this study was to determine if newly designed metalloporphyrins have enhanced pharmacodynamics including oral bioavailability, longer plasma elimination half-lives, penetrate the blood brain barrier, and show promise for PD treatment. Three metalloporphyrins (AEOL 11216, AEOL 11203 and AEOL 11114) were identified in this study as potential candidates for further pre-clinical development. Each of these compounds demonstrated blood brain barrier permeability by the i.p. route and two of three compounds (AEOL 11203 and AEOL 11114) were orally bioavailable. All of these compounds protected against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity, including dopamine depletion in the striatum, dopaminergic neuronal loss in the substantial nigra, and increased oxidative/nitrative stress indices (glutathione disulfide and 3-nitrotyrosine) in the ventral midbrain of the mice without inhibiting MPTP metabolism. Daily therapeutic dosing of these metalloporphyrins were well tolerated without accumulation of brain manganese levels or behavioral alterations assessed by open field and rotarod tests. The study identified two orally active metalloporphyrins and one injectable metalloporphyrin as clinical candidates for further development in PD.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Antiparkinsonianos/farmacologia
Encéfalo/efeitos dos fármacos
Intoxicação por MPTP/prevenção & controle
Metaloporfirinas/farmacologia
Fármacos Neuroprotetores/farmacologia
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina
Administração Oral
Animais
Antioxidantes/administração & dosagem
Antioxidantes/farmacocinética
Antiparkinsonianos/administração & dosagem
Antiparkinsonianos/farmacocinética
Comportamento Animal/efeitos dos fármacos
Disponibilidade Biológica
Biomarcadores/metabolismo
Barreira Hematoencefálica/metabolismo
Encéfalo/metabolismo
Encéfalo/fisiopatologia
Permeabilidade Capilar
Modelos Animais de Doenças
Dopamina/metabolismo
Desenho de Drogas
Avaliação Pré-Clínica de Medicamentos
Meia-Vida
Injeções Intraperitoneais
Intoxicação por MPTP/etiologia
Intoxicação por MPTP/metabolismo
Intoxicação por MPTP/fisiopatologia
Masculino
Metaloporfirinas/administração & dosagem
Metaloporfirinas/farmacocinética
Camundongos Endogâmicos C57BL
Atividade Motora/efeitos dos fármacos
Fármacos Neuroprotetores/administração & dosagem
Fármacos Neuroprotetores/farmacocinética
Teste de Desempenho do Rota-Rod
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Antiparkinson Agents); 0 (Biomarkers); 0 (Metalloporphyrins); 0 (Neuroprotective Agents); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170413
[St] Status:MEDLINE


  7 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28364506
[Au] Autor:Nagai H; de Vivo L; Bellesi M; Ghilardi MF; Tononi G; Cirelli C
[Ad] Endereço:Department of Psychiatry, University of Wisconsin-Madison, 6001 Research Park Blvd, Madison, WI 53719.
[Ti] Título:Sleep Consolidates Motor Learning of Complex Movement Sequences in Mice.
[So] Source:Sleep;40(2), 2017 Feb 01.
[Is] ISSN:1550-9109
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Introduction: Sleep-dependent consolidation of motor learning has been extensively studied in humans, but it remains unclear why some, but not all, learned skills benefit from sleep. Aims and Methods: Here, we compared 2 different motor tasks, both requiring the mice to run on an accelerating device. In the rotarod task, mice learn to maintain balance while running on a small rod, while in the complex wheel task, mice run on an accelerating wheel with an irregular rung pattern. Results: In the rotarod task, performance improved to the same extent after sleep or after sleep deprivation (SD). Overall, using 7 different experimental protocols (41 sleep deprived mice, 26 sleeping controls), we found large interindividual differences in the learning and consolidation of the rotarod task, but sleep before/after training did not account for this variability. By contrast, using the complex wheel, we found that sleep after training, relative to SD, led to better performance from the beginning of the retest session, and longer sleep was correlated with greater subsequent performance. As in humans, the effects of sleep showed large interindividual variability and varied between fast and slow learners, with sleep favoring the preservation of learned skills in fast learners and leading to a net offline gain in the performance in slow learners. Using Fos expression as a proxy for neuronal activation, we also found that complex wheel training engaged motor cortex and hippocampus more than the rotarod training. Conclusions: Sleep specifically consolidates a motor skill that requires complex movement sequences and strongly engages both motor cortex and hippocampus.
[Mh] Termos MeSH primário: Aprendizagem/fisiologia
Consolidação da Memória/fisiologia
Destreza Motora/fisiologia
Sono/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Hipocampo/fisiologia
Masculino
Camundongos
Córtex Motor/fisiologia
Teste de Desempenho do Rota-Rod
Privação do Sono/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170402
[St] Status:MEDLINE
[do] DOI:10.1093/sleep/zsw059


  8 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:28355345
[Au] Autor:Salazar-Juárez A; Barbosa-Méndez S; Merino-Reyes P; Matus-Ortega M; Hernández-Calderón JA; Antón B
[Ad] Endereço:Laboratorio de Neurobiología Molecular y Neuroquímica de Adicciones, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Mexico City, Mexico.
[Ti] Título:Chronic dosing with mirtazapine does not produce sedation in rats.
[So] Source:Rev Bras Psiquiatr;39(3):228-236, 2017 Jul-Sep.
[Is] ISSN:1809-452X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Objective:: Sedation/somnolence are major side effects of pharmacotherapies for depression, and negatively affect long-term treatment compliance in depressed patients. Use of mirtazapine (MIR), an atypical antidepressant approved for the treatment of moderate to severe depression with comorbid anxiety disorders, is associated with significant sedation/somnolence, especially in short-term therapy. Nonetheless, studies with human subjects suggest that MIR-induced sedation is transient, especially when high and repeated doses are used. The purpose of this study was to explore the effects of acute and chronic administration of different doses of MIR on sedation in the rat. Methods:: Assessment of sedation was carried out behaviorally using the rotarod, spontaneous locomotor activity, and fixed-bar tests. Results:: A 15-mg/kg dose of MIR induced sedative effects for up to 60 minutes, whereas 30 mg/kg or more produced sedation within minutes and only in the first few days of administration. Conclusion:: These results suggest that 30 mg/kg is a safe, well-tolerated dose of MIR which generates only temporary sedative effects.
[Mh] Termos MeSH primário: Antidepressivos Tricíclicos/farmacologia
Hipnóticos e Sedativos/farmacologia
Locomoção/efeitos dos fármacos
Mianserina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antidepressivos Tricíclicos/administração & dosagem
Peso Corporal/efeitos dos fármacos
Relação Dose-Resposta a Droga
Masculino
Mianserina/administração & dosagem
Mianserina/farmacologia
Ratos Wistar
Teste de Desempenho do Rota-Rod/métodos
Fatores de Tempo
Trazodona/administração & dosagem
Trazodona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents, Tricyclic); 0 (Hypnotics and Sedatives); 250PJI13LM (Mianserin); A051Q2099Q (mirtazapine); YBK48BXK30 (Trazodone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE


  9 / 1313 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28238857
[Au] Autor:Gopi M; Arambakkam Janardhanam V
[Ad] Endereço:Department of Biochemistry, University of Madras, Guindy Campus, Chennai 600 025, Tamilnadu, India. Electronic address: gopibio89@gmail.com.
[Ti] Título:Asiaticoside: Attenuation of rotenone induced oxidative burden in a rat model of hemiparkinsonism by maintaining the phosphoinositide-mediated synaptic integrity.
[So] Source:Pharmacol Biochem Behav;155:1-15, 2017 Apr.
[Is] ISSN:1873-5177
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Asiaticoside (AS), a triterpenoid saponin isolated from the Indian medicinal herb Centella asiatica is known to exert a neuroprotective effect by attenuating the neurobehavioral, neurochemical and pathological changes in animal models. However, its potential neuroprotection in rotenone-induced hemiparkinsonism which implicates phospholipid-mediated neurotransmission remains unclear. Therefore, we have investigated the neuroprotective effects of AS in rat model of ROT-infused hemiparkinsonism with respect to phosphoinositides-assisted cytodynamics and synaptic function. Adult male Sprague-Dawley rats (250-300g) were distributed randomly into 6 groups, with 6 rats in each group: Sham control, Vehicle control (DMSO-0.1%), ROT-infused group (6µg/µl/kg), AS-treated group (50mg/kg/day), Drug (AS) control and Levodopa (l-DOPA)-treated group (6mg/kg/day). At the end of the experimental period, the rats were sacrificed after performing behavioral analyses and the striatum regions were dissected out. Phosphoinositides (PI) are involved in intrinsic membrane signals that regulate intracellular membrane trafficking vesicle and endocytosis. We have assessed mRNA and protein expressions of genes involved in PI-mediated signaling and also in synaptic function (PI3K, PDK 1, PEBP, Stx 1A and TH) in addition to the levels of neurotransmitters and the enzymatic antioxidant profile. AS caused an improved working memory and motor co-ordination in the ROT group. It alters the levels of neurotransmitters (p<0.01), the expression of mRNA and protein assessed which were significantly affected (P<0.001) by rotenone, thus exhibiting its intervention in the progression of neurodegeneration. We demonstrate that AS can mediate distinct function in PI-assisted vesicle endocytosis, cytoprotective signaling and in the synaptic function thereby mitigating the ROT-infused hemiparkinsonism, however, its specific regulatory role remains to be unraveled.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Estresse Oxidativo/efeitos dos fármacos
Transtornos Parkinsonianos/prevenção & controle
Fosfatidilinositóis/metabolismo
Rotenona/farmacologia
Sinapses/efeitos dos fármacos
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Western Blotting
Cromatografia Líquida de Alta Pressão
Masculino
Aprendizagem em Labirinto
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/metabolismo
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Teste de Desempenho do Rota-Rod
Sinapses/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphatidylinositols); 0 (Triterpenes); 03L9OT429T (Rotenone); PKO39VY215 (asiaticoside)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170228
[St] Status:MEDLINE


  10 / 1313 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28178592
[Au] Autor:Gill JS; Jamwal S; Kumar P; Deshmukh R
[Ad] Endereço:Neuropharmacology Division, Department of Pharmacology, I.S.F College of Pharmacy, Moga, Punjab, India.
[Ti] Título:Sertraline and venlafaxine improves motor performance and neurobehavioral deficit in quinolinic acid induced Huntington's like symptoms in rats: Possible neurotransmitters modulation.
[So] Source:Pharmacol Rep;69(2):306-313, 2017 Apr.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Huntington Disease is autosomal, fatal and progressive neurodegenerative disorder for which clinically available drugs offer only symptomatic relief. Emerging strides have indicated that antidepressants improve motor performance, restore neurotransmitters level, ameliorates striatal atrophy, increases BDNF level and may enhance neurogenesis. Therefore, we investigated sertraline and venlafaxine, clinically available drugs for depression with numerous neuroprotective properties, for their beneficial effects, if any, in quinolinic acid induced Huntington's like symptoms in rats. METHODS: Rats were administered quinolinic acid (QA) (200 nmol/2µl saline) intrastriatal bilaterally on 0day. Sertraline and venlafaxine (10 and 20mg/kg, po) each were administered for 21days once a day. Motor performance was assessed using rotarod test, grip strength test, narrow beam walk test on weekly basis. On day 22, animals were sacrificed and rat striatum was isolated for biochemical (LPO, GSH and Nitrite), neuroinflammation (TNF-α, IL-1ß and IL-6) and neurochemical analysis (GABA, glutamate, norepinephrine, dopamine, serotonin, DOPAC, HVA and 5-HIAA). RESULTS: QA treatment significantly altered body weight, motor performance, oxidative defense (increased LPO, nitrite and decreased GSH), pro-inflammatory cytokines levels (TNF-α, IL-6 and IL-1ß), neurochemical level (GABA, glutamate, nor-epinephrine, dopamine, serotonin, HVA, DOPAC, 5-HIAA). Sertraline and venlafaxine at selected doses significantly attenuated QA induced alterations in striatum. CONCLUSION: The present study suggests that modulation of monoamines level, normalization of GABA and glutamatergic signaling, anti-oxidant and anti-inflammatory properties could underlie the neuroprotective effect of sertraline and venlafaxine in QA induced Huntington's like symptoms.
[Mh] Termos MeSH primário: Doença de Huntington/induzido quimicamente
Doença de Huntington/tratamento farmacológico
Atividade Motora/efeitos dos fármacos
Neurotransmissores/metabolismo
Ácido Quinolínico/farmacologia
Sertralina/farmacologia
Cloridrato de Venlafaxina/farmacologia
[Mh] Termos MeSH secundário: Animais
Corpo Estriado/efeitos dos fármacos
Corpo Estriado/metabolismo
Modelos Animais de Doenças
Ácido Glutâmico/metabolismo
Doença de Huntington/metabolismo
Interleucina-1beta/metabolismo
Interleucina-6/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Fármacos Neuroprotetores/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Wistar
Teste de Desempenho do Rota-Rod/métodos
Fator de Necrose Tumoral alfa/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Interleukin-6); 0 (Neuroprotective Agents); 0 (Neurotransmitter Agents); 0 (Tumor Necrosis Factor-alpha); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); 7D7RX5A8MO (Venlafaxine Hydrochloride); F6F0HK1URN (Quinolinic Acid); QUC7NX6WMB (Sertraline)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE



página 1 de 132 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde