Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/199682
Type: Artigo de periódico
Title: Glatiramer Acetate Treatment Increases Stability Of Spinal Synapses And Down Regulates Mhc I During The Course Of Eae.
Author: Scorisa, Juliana M
Freria, Camila M
Victorio, Sheila C
Barbizan, Roberta
Zanon, Renata G
Oliveira, Alexandre L R
Abstract: The 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 (0.05 mg/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.
Subject: Analysis Of Variance
Animals
Blotting, Western
Encephalomyelitis, Autoimmune, Experimental
Female
Gene Expression Regulation
Genes, Mhc Class I
Immunohistochemistry
Mice
Mice, Inbred C57bl
Microscopy, Electron, Transmission
Peptides
Spinal Cord
Synapses
Eae
Mhc Class I
Glatiramer Acetate.
Immunomodulator
Motoneuron
Spinal Cord
Rights: aberto
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/22043176
Date Issue: 2011
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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