Spermine reverses lipopolysaccharide-induced memory deficit in mice.

Autor: Frühauf PK; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. pam_fruhauf@yahoo.com.br., Ineu RP; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. rafaelineu@gmail.com., Tomazi L; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. ledianetomazi@gmail.com., Duarte T; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. duartethiago89@yahoo.com.br., Mello CF; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. cf.mello@smail.ufsm.br.; Department of Physiology and Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. cf.mello@smail.ufsm.br., Rubin MA; Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. maribel.rubin@gmail.com.; Department of Biochemistry and Molecular Biology, Natural and Exact Sciences Center, Federal University of Santa Maria, Camobi, CEP: 97105900, Santa Maria, RS, Brazil. maribel.rubin@gmail.com.
Jazyk: angličtina
Zdroj: Journal of neuroinflammation [J Neuroinflammation] 2015 Jan 09; Vol. 12, pp. 3. Date of Electronic Publication: 2015 Jan 09.
DOI: 10.1186/s12974-014-0220-5
Abstrakt: Background: Lipopolysaccharide (LPS) induces neuroinflammation and memory deficit. Since polyamines improve memory in various cognitive tasks, we hypothesized that spermine administration reverses LPS-induced memory deficits in an object recognition task in mice. The involvement of the polyamine binding site at the N-methyl-D-aspartate (NMDA) receptor and cytokine production in the promnesic effect of spermine were investigated.
Methods: Adult male mice were injected with LPS (250 μg/kg, intraperitoneally) and spermine (0.3 to 1 mg/kg, intraperitoneally) or ifenprodil (0.3 to 10 mg/kg, intraperitoneally), or both, and their memory function was evaluated using a novel object recognition task. In addition, cortical and hippocampal cytokines levels were measured by ELISA four hours after LPS injection.
Results: Spermine increased but ifenprodil decreased the recognition index in the novel object recognition task. Spermine, at doses that did not alter memory (0.3 mg/kg, intraperitoneally), reversed the cognitive impairment induced by LPS. Ifenprodil (0.3 mg/kg, intraperitoneally) reversed the protective effect of spermine against LPS-induced memory deficits. However, spermine failed to reverse the LPS-induced increase of cortical and hippocampal cytokine levels.
Conclusions: Spermine protects against LPS-induced memory deficits in mice by a mechanism that involves GluN2B receptors.
Databáze: MEDLINE