Advanced search
Start date
Betweenand
Related content
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Spermine protects from LPS-induced memory deficit via BDNF and TrkB activation

Full text
Author(s):
Fruhauf-Perez, Pamella K. [1] ; Temp, Fernanda R. [1] ; Pillat, Micheli M. [2] ; Signor, Cristiane [3] ; Wendel, Arithane Lorena [3] ; Ulrich, Henning [2] ; Mello, Carlos F. [1] ; Rubin, Maribel A. [1, 3]
Total Authors: 8
Affiliation:
[1] Univ Fed Santa Maria, Ctr Hlth Sci, Grad Program Pharmacol, Santa Maria, RS - Brazil
[2] Univ Sao Paulo, Chem Inst, Biochem Dept, BR-05508900 Sao Paulo - Brazil
[3] Univ Fed Santa Maria, Ctr Neural & Exact Sci, Grad Program Biol Sci Toxicol Biochem, Santa Maria, RS - Brazil
Total Affiliations: 3
Document type: Journal article
Source: NEUROBIOLOGY OF LEARNING AND MEMORY; v. 149, p. 135-143, MAR 2018.
Web of Science Citations: 6
Abstract

Lipopolysaccharide (LPS) has been long known to promote neuroinflammation and learning and memory deficits. Since spermine, one of the main natural polyamines in the central nervous system, protects from LPS-induced memory deficit by a mechanism that comprises GluN2B receptors, the aim of the present study was to determine whether brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB) receptor and cAMP response element binding (CREB) are involved in this protective effect of spermine. Adult male Swiss albino mice received, immediately after training in the novel object recognition task, saline or LPS (250 mu g/kg, i.p.); 5 min later they received saline or spermine (0.3 mg/kg, i.p.) and, when specified, 5 min thereafter saline or the TrkB receptor antagonist ANA-12 (0.5 mg/kg, i.p.) in different flanks. Animals were tested 24h after training. Spermine protected from LPS-induced memory deficit and this protective effect was reversed by ANA-12. In a subset of animals BDNF, CREB and phospho-CREB immunoreactivity was determined in the hippocampi and cerebral cortex 4 h after spermine injection. Spermine reversed the decrease of mature BDNF levels induced by LPS in both hippocampus and cerebral cortex. Spermine increased phospho-CREB content and phospho-CREB/total CREB ratio in the cerebral cortex of LPS-treated mice. The results support that the protective effect of spermine on LPS-induced memory deficits depends on TrkB receptor activation and is accompanied by restoration of mature BDNF levels in hippocampus and cerebral cortex, as well as increased CREB phosphorylation in the cerebral cortex. (AU)

FAPESP's process: 15/19478-3 - Role of kinin-B2 receptor in pathogenesis and progression of familial Alzheimer's Disease: from neurogenesis and immune response to cognition
Grantee:Micheli Mainardi Pillat
Support type: Scholarships in Brazil - Post-Doctorate