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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.
Insights
Spermine administration reverses lipopolysaccharide-induced memory deficits in mice. This effect involves GluN2B receptors, suggesting a potential therapeutic strategy for neuroinflammation-related cognitive impairment.
Area of Science:
- Neuroscience
- Pharmacology
- Cognitive Science
Background:
- Lipopolysaccharide (LPS) is known to induce neuroinflammation and memory deficits.
- Polyamines, such as spermine, have shown potential in improving memory across various cognitive tasks.
- This study investigates spermine's ability to counteract LPS-induced memory impairment.
Purpose of the Study:
- To determine if spermine administration can reverse memory deficits caused by LPS in mice.
- To explore the role of the N-methyl-D-aspartate (NMDA) receptor's polyamine binding site in spermine's pro-cognitive effects.
- To assess the impact of spermine on cytokine production in the context of LPS-induced neuroinflammation.
Main Methods:
- Adult male mice were administered LPS and varying doses of spermine or ifenprodil.
- Memory function was assessed using a novel object recognition task.
- Cortical and hippocampal cytokine levels were measured via ELISA.
Main Results:
- Spermine administration improved the recognition index in the object recognition task.
- Spermine effectively reversed LPS-induced cognitive impairment at specific doses.
- Ifenprodil partially blocked spermine's protective effects against LPS-induced memory deficits.
- Spermine did not significantly alter LPS-induced increases in cortical and hippocampal cytokine levels.
Conclusions:
- Spermine demonstrates a protective effect against LPS-induced memory deficits in mice.
- The mechanism of spermine's action appears to involve GluN2B receptors.
- Spermine's pro-cognitive effects in this model are not mediated by a reduction in neuroinflammatory cytokines.
