Spermine reverses lipopolysaccharide-induced memory deficit in mice

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. © frühauf et al.; licensee biomed central.