Memory persistence needs a new event of consolidation 12h after the acquisition. We investigated the role of the cholinergic activity on the persistence of memory. For this purpose, we performed the treatments 9 or 12h after acquisition and the memory tested 2 or 7 days after inhibitory avoidance (IA) training. Here we report that activity of medial septum, by transitorily inactivating this structure with lidocaine 12h after IA training, is essential for memory persistence at the 7th day, but not for the formation at the 2nd day. We also report that muscarinic and nicotinic cholinergic receptors of CA1 area are engaged on memory persistence. Since scopolamine (mAChRs antagonist) and mecamylamine (nAChRs blocker) infusions, 12h post-training, demonstrated impairment on long term memory (LTM), persistence on the 7th day but no effect on LTM formation was found on the 2nd day in the IA test. The same effects were found with pirenzepine, an M1 antagonist. No effects on the formation and persistence of memory on the 2nd and 7th days were demonstrated after DHβE infusions (nAChRs subtype antagonist α4β2, α3β2). These findings suggest that mAChR and nAChR at the CA1 area, and also MS activation, are required for the persistence of memory.

Memory persistence in the inhibitory avoidance (IA) task has been recently shown to require a new event of consolidation 12 hr after acquisition. The immobilization stress (IS) model is largely used to study the effects of stress on memory. In this study we investigated the interactions between stress by immobilization and its effect on the persistence of memory, and also a possible effect mediated by β-adrenergic modulation of stress on memory persistence. An enhancement of long-term memory (LTM) persistence caused by stress through immobilization applied 12 hr after IA training was observed when the animals were submitted to 15 min or 1 hr of IS, but not to 3 hr. The reversal of this memory enhancement caused by IS was observed when the β-adrenergic antagonist propranolol was infused intraperitoneally prior to stress, which implies that β-adrenergic receptors are involved in stress enhancement of LTM persistence.