dc.creatorScorisa, JM
dc.creatorFreria, CM
dc.creatorVictorio, SC
dc.creatorBarbizan, R
dc.creatorZanon, RG
dc.creatorOliveira, ALR
dc.date2011
dc.date2014-07-30T17:48:00Z
dc.date2015-11-26T17:48:25Z
dc.date2014-07-30T17:48:00Z
dc.date2015-11-26T17:48:25Z
dc.date.accessioned2018-03-29T00:31:17Z
dc.date.available2018-03-29T00:31:17Z
dc.identifierInternational Journal Of Biological Sciences. Ivyspring Int Publ, v. 7, n. 8, n. 1188, n. 1202, 2011.
dc.identifier1449-2288
dc.identifierWOS:000298010400010
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/68072
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/68072
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1289085
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionThe recent discovery that the major histocompatibility complex of class I (MHC I) expression has a role in the synaptic elimination process, represented an insight into understanding the cross talk between neurons. In the present study, the possibility that glatiramer acetate (GA) treatment influences the MHC class I expression and the synaptic plasticity process in the spinal cord during the course of EAE was investigated. C57BL/6J mice were induced to EAE and submitted to treatment either with a placebo solution or with GA (0.05mg/animal, subcutaneously, on a daily basis). All the animals were sacrificed at the peak disease (14 days after induction) or at the point of recovery of the clinical signs (21 days after induction). The spinal cords were removed and submitted to immunohistochemical examination, Western blotting and transmission electron microscopy analysis. The results showed that GA treatment was able to decrease synaptic loss during the course of EAE, which correlates with the downregulation of the MHC I complex. The present results reinforce the neuroprotective role of GA treatment, by reducing synaptic loss during the course of the disease. Such action may be associated with the recently described role of MHC I regulation during the synaptic plasticity process.
dc.description7
dc.description8
dc.description1188
dc.description1202
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFAPESP [2011/18991-8]
dc.languageen
dc.publisherIvyspring Int Publ
dc.publisherLake Haven
dc.publisherAustralia
dc.relationInternational Journal Of Biological Sciences
dc.relationInt. J. Biol. Sci.
dc.rightsaberto
dc.sourceWeb of Science
dc.subjectEAE
dc.subjectMHC class I
dc.subjectspinal cord
dc.subjectmotoneuron
dc.subjectimmunomodulator
dc.subjectglatiramer acetate
dc.subjectExperimental Autoimmune Encephalomyelitis
dc.subjectMotoneuron Synaptic Plasticity
dc.subjectT-cell Responses
dc.subjectMultiple-sclerosis
dc.subjectAnimal-model
dc.subjectExpression
dc.subjectPeptide
dc.subjectNeurons
dc.subjectGene
dc.subjectRegeneration
dc.titleGlatiramer Acetate Treatment Increases Stability of Spinal Synapses and Down Regulates MHC I during the Course of EAE
dc.typeArtículos de revistas


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