In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT.

No abstract

No abstract

Lipopolysaccharide (LPS) has been long known to promote neuroinflammation and learning and memory deficits. Since spermine, one of the main natural polyamines in the central nervous system, protects from LPS-induced memory deficit by a mechanism that comprises GluN2B receptors, the aim of the present study was to determine whether brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB) receptor and cAMP response element binding (CREB) are involved in this protective effect of spermine. Adult male Swiss albino mice received, immediately after training in the novel object recognition task, saline or LPS (250 μg/kg, i.p.); 5 min later they received saline or spermine (0.3 mg/kg, i.p.) and, when specified, 5 min thereafter saline or the TrkB receptor antagonist ANA-12 (0.5 mg/kg, i.p.) in different flanks. Animals were tested 24 h after training. Spermine protected from LPS-induced memory deficit and this protective effect was reversed by ANA-12. In a subset of animals BDNF, CREB and phospho-CREB immunoreactivity was determined in the hippocampi and cerebral cortex 4 h after spermine injection. Spermine reversed the decrease of mature BDNF levels induced by LPS in both hippocampus and cerebral cortex. Spermine increased phospho-CREB content and phospho-CREB/total CREB ratio in the cerebral cortex of LPS-treated mice. The results support that the protective effect of spermine on LPS-induced memory deficits depends on TrkB receptor activation and is accompanied by restoration of mature BDNF levels in hippocampus and cerebral cortex, as well as increased CREB phosphorylation in the cerebral cortex.

Persistence is the most characteristic attribute of long-term memory (LTM). For memory persistence, a second late event of consolidation, that occurs around 12h after the acquisition, is necessary. Although the N-methyl-d-aspartate (NMDA) receptor has been involved in the persistence of memory, whether endogenous modulators of the NMDA receptor actually modulate memory persistence is unknown. In the current study we investigated whether spermidine and arcaine, respectively agonist and antagonist of polyamine binding site at NMDA receptor, alter the persistence of the memory of contextual fear conditioning task in rats. While 12h post-training administration of spermidine (10 and 30mg/kg, i.p.) facilitated, arcaine (10mg/kg, i.p.) impaired the memory of fear assessed 2 and 7 days after training. Arcaine (0.1mg/kg) prevented the facilitatory effect of spermidine (10mg/kg, i.p.), and spermidine (1mg/kg), prevented the memory impairment induced by arcaine (10mg/kg, i.p.) when tested 2 and 7 days after training. These results suggest that endogenous polyamines improve the persistence of fear memory.