Participation of hippocampal cholinergic system in memory persistence for inhibitory avoidance in rats

Abstract

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 reconsolidation and its maintenance depend on L-voltage-dependent calcium channels and CaMKII functions regulating protein turnover in the hippocampus

“…M emory maintenance or persistence depends on the degree of emotional arousal present at the time of consolidation (1, 2), and apparently on several different biochemical and behavioral variables over the next several hours or days (3)(4)(5)(6)(7)(8)(9), especially in the hippocampus, which is widely recognized as the region in charge of consolidation and maintenance (10)(11)(12)(13). An important factor in memory maintenance is reconsolidation (14)(15)(16), which originates in the labilization of memories caused by nonreinforced retrieval.…”

Critical Role of CA1 Nicotinic Receptors on Memory Acquisition Deficit Under Induction of Total Sleep Deprivation and REM Sleep Deprivation

“…21 Posterior hippocampus or CA1 which has a significant role in learning and memory includes high amounts of cholinergic receptors. 25 In the present study, both TSDs and RSDs are expected to reduce memory acquisition, activate nAchRs of hippocampus CA1 area, provide suitable conditions for neuronal plasticizing and LTP production, and improve memory acquisition, and since the concentration of Ach increases during the RAM sleep and decreases during NREM sleep, 20 and given the fact that there is RSD in the TSD as well, it is also possible that the 2 groups respond similarly to the activation of nAchRs.…”

New frontiers in the study of memory mechanisms

“…Notwithstanding this, several recent studies have implicated the hippocampus in the initiation of ''permanent'' memory storage, in some cases through local biochemical changes. [28][29][30][31][32][33] These biochemical changes involve the production of local BDNF 28,29 and/or the local activation of a circadian cycle of simultaneous increases of hippocampal mitogen-activated protein kinase (MAPK) activity and cyclic adenosine monophosphate (cAMP), 30,31 and/or the triggering of a dual muscarinic and nicotinic cholinergic mechanism within the hippocampus, 32 or the participation of a hippocampal b-noradrenergic mechanism activated by mild stress, presumably that of the training experience. 33 The BDNF mechanism appears to be triggered by dopaminergic fibers from the ventral tegmental area acting on hippocampal D1 receptors.…”

“…33 The BDNF mechanism appears to be triggered by dopaminergic fibers from the ventral tegmental area acting on hippocampal D1 receptors. 30,31 Interestingly, all these mechanisms have been proposed to enter into play several hours after training, when the ensuing cellular consolidation process are already over, [28][29][30][31][32][33][34][35] and they are not mutually incompatible, which means they might occur simultaneously and eventually interact with each other in the fostering of memory persistence.…”

“…The two human hippocampi together have at least 400 million pyramidal cells, each receiving about 10,000 synapses, which makes it an apparatus with potentially formidable, though not infinite, synaptic processing properties. If specific connections between the hippocampal synapses that are involved in consolidation [28][29][30][31][32][33] and those that house their more permanent storage forms 25,27 exist, they must be modest in size and number.…”