Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis

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dc.contributorLaboratório de Dor e Sinalizaçãopt_BR
dc.contributor.authorTeixeira, Nathália Bernardespt_BR
dc.contributor.authorPicolo, Giselept_BR
dc.contributor.authorGiardini, Aline Carolinapt_BR
dc.contributor.authorBoumezbeur, Fawzipt_BR
dc.contributor.authorPottier, Géraldinept_BR
dc.contributor.authorKuhnast, Bertrandpt_BR
dc.contributor.authorServent, Denispt_BR
dc.contributor.authorBenoit, Evelynept_BR
dc.identifier.citationTeixeira NB, Picolo G, Giardini AC, Boumezbeur F, Pottier G, Kuhnast B, et al. Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis. J. Neuroinflammation. 2020 Sep;17:266. doi:10.1186/s12974-020-01936-9.pt_BR
dc.description.abstractBackground Experimental autoimmune encephalomyelitis (EAE) is the most commonly used and clinically relevant murine model for human multiple sclerosis (MS), a demyelinating autoimmune disease characterized by mononuclear cell infiltration into the central nervous system (CNS). The aim of the present study was to appraise the alterations, poorly documented in the literature, which may occur at the peripheral nervous system (PNS) level. Methods To this purpose, a multiple evaluation of peripheral nerve excitability was undertaken, by means of a minimally invasive electrophysiological method, in EAE mice immunized with the myelin oligodendrocyte glycoprotein (MOG) 35-55 peptide, an experimental model for MS that reproduces, in animals, the anatomical and behavioral alterations observed in humans with MS, including CNS inflammation, demyelination of neurons, and motor abnormalities. Additionally, the myelin sheath thickness of mouse sciatic nerves was evaluated using transmission electronic microscopy. Results As expected, the mean clinical score of mice, daily determined to describe the symptoms associated to the EAE progression, increased within about 18 days after immunization for EAE mice while it remained null for all control animals. The multiple evaluation of peripheral nerve excitability, performed in vivo 2 and 4 weeks after immunization, reveals that the main modifications of EAE mice, compared to control animals, are a decrease of the maximal compound action potential (CAP) amplitude and of the stimulation intensity necessary to generate a CAP with a 50% maximum amplitude. In addition, and in contrast to control mice, at least 2 CAPs were recorded following a single stimulation in EAE animals, reflecting various populations of sensory and motor nerve fibers having different CAP conduction speeds, as expected if a demyelinating process occurred in the PNS of these animals. In contrast, single CAPs were always recorded from the sensory and motor nerve fibers of control mice having more homogeneous CAP conduction speeds. Finally, the myelin sheath thickness of sciatic nerves of EAE mice was decreased 4 weeks after immunization when compared to control animals. Conclusions In conclusion, the loss of immunological self-tolerance to MOG in EAE mice or in MS patients may not be only attributed to the restricted expression of this antigen in the immunologically privileged environment of the CNS but also of the PNS.pt_BR
dc.description.sponsorship(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.description.sponsorship(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.relation.ispartofJournal of Neuroinflammationpt_BR
dc.rightsOpen accesspt_BR
dc.titleAlterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosispt_BR
dc.contributor.externalUniversité Paris-Saclaypt_BR
dc.subject.keywordExperimental autoimmune encephalomyelitispt_BR
dc.subject.keywordMultiple sclerosispt_BR
dc.subject.keywordMyelin oligodendrocyte glycoproteinpt_BR
dc.subject.keywordNeuromuscular junctionpt_BR
dc.subject.keywordPeripheral nervous systempt_BR
dc.relation.ispartofabbreviatedJ Neuroinflammationpt_BR
dc.identifier.citationabntv. 17, 266, set. 2020pt_BR
dc.identifier.citationvancouver2020 Sep;17:266pt_BR
dc.contributor.butantanTeixeira, Nathália Bernardes|:Aluno|:Laboratório de Dor e Sinalização|:PrimeiroAutorpt_BR
dc.contributor.butantanPicolo, Gisele|:Pesquisador:Docente Permanente PPGTOX|:Laboratório de Dor e Sinalizaçãopt_BR
dc.contributor.butantanGiardini, Aline Carolina|:Aluno|:Laboratório de Dor e Sinalizaçãopt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2011/17974-2pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦2013/07467-1pt_BR
dc.sponsorship.butantan(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior¦¦001pt_BR
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