Espermina reverte o dano de memória induzido por lipopolissacarídeo em camundongos

Abstract

Neuroinflammation is a neuropathological finding in a number of neurodegenerative diseases. Intraperitoneal injection of lipopolysaccharide (LPS) induces neuroinflammation and memory deficit. Spermine and spermidine are endogenous polyamines that physiologically modulate the N-methyl-D-aspartate (NMDA) receptor in mammals by binding to the polyamine-binding site at the NMDA receptor. Since polyamines improve memory in cognitive tasks, we tested whether the post-training administration of spermine reverses the deficits of memory induced by LPS in the object recognition task in mice. While spermine (1 mg/kg, i.p.) increased, ifenprodil (10 mg/kg, i.p.), a noncompetitive GluN2B-containing NMDA receptor antagonist, decreased the discrimination score on novel object recognition task. Spermine, at dose that did not alter memory (0.3 mg/kg, i.p.), reversed the cognitive impairment induced by LPS (250 μg/kg, i.p.). Ifenprodil (0.3 mg/kg, i.p.) reversed the protective effect of spermine against LPS-induced memory deficits in the novel object recognition task. However, spermine failed to reverse the LPS-induced increased of cortical and hippocampal cytokines levels. The results indicate that spermine protects from LPS-induced memory deficits in mice by mechanisms other than decreasing LPS-induced cytokine production.