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Spermine reverses lipopolysaccharide-induced memory deficit in mice
Pâmella Karina Santana Frühauf1, Rafael Porto Ineu2, Lediane Tomazi3
1Graduation Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS, 97105-900, Brazil. pam_fruhauf@yahoo.com.br.
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.
