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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

High dose of dexamethasone protects against EAE-induced motor deficits but impairs learning/memory in C57BL/6 mice

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dos Santos, Nilton [1] ; Novaes, Leonardo S. [1] ; Dragunas, Guilherme [1] ; Rodrigues, Jennifer R. [1] ; Brandao, Wesley [2] ; Camarini, Rosana [1] ; Schatzmann Peron, Jean Pierre [2] ; Demarchi Munhoz, Carolina [1]
Total Authors: 8
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, BR-05508000 Sao Paulo - Brazil
Total Affiliations: 2
Document type: Journal article
Source: SCIENTIFIC REPORTS; v. 9, APR 30 2019.
Web of Science Citations: 1

Multiple sclerosis (MS) is an autoimmune and neuroinflammatory disease characterized by demyelination of the Central Nervous System. Immune cells activation and release of pro-inflammatory cytokines play a crucial role in the disease modulation, decisively contributing to the neurodegeneration observed in MS and the experimental autoimmune encephalomyelitis (EAE), the widely used MS animal model. Synthetic glucocorticoids, commonly used to treat the MS attacks, have controversial effects on neuroinflammation and cognition. We sought to verify the influence of dexamethasone (DEX) on the EAE progression and on EAE-induced cognitive deficits. In myelin oligodendrocyte glycoprotein peptide (MOG35-55)-induced EAE female mice, treated once with DEX (50 mg/kg) or not, on the day of immunization, DEX decreased EAE-induced motor clinical scores, infiltrating cells in the spinal cord and delayed serum corticosterone peak. At the asymptomatic phase (8-day post-immunization), DEX did not protected from the EAE-induced memory consolidation deficits, which were accompanied by increased glucocorticoid receptor (GR) activity and decreased EGR-1 expression in the hippocampus. Blunting hippocampal GR genomic activation with DnGR vectors prevented DEX effects on EAE-induced memory impairment. These data suggest that, although DEX improves clinical signs, it decreases cognitive and memory capacity by diminishing neuronal activity and potentiating some aspects of neuroinflammation in EAE. (AU)

FAPESP's process: 12/24727-4 - Comparison of the therapeutical effects of dexamethasone (a synthetic glucocorticoid analogue), and G1 (a G-coupled estrogen receptor, GPER agonist) on the EAE-induced neuroinflammation
Grantee:Carolina Demarchi Munhoz
Support type: Regular Research Grants
FAPESP's process: 12/24002-0 - Effects of environmental enrichment in long-lasting anxiety symptoms triggered by acute stress: implications in the emotional memory acquisition
Grantee:Leonardo Santana Novaes
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 16/03572-3 - The relationship between glucocorticoid receptor activation and the neuronal hyperexcitability in the basolateral amygdala in the restraint stress-induced long-lasting anxiety and their implications in the impaired contextual fear extinction
Grantee:Carolina Demarchi Munhoz
Support type: Regular Research Grants
FAPESP's process: 11/18703-2 - The role of Indoleamine-2,3-dioxigenase and the Triptophan - Kynurenines axis through NMDA receptors over the immune response in the EAE and stroke model
Grantee:Jean Pierre Schatzmann Peron
Support type: Research Grants - Young Investigators Grants