Plastic modifications induced by object recognition memory processing

Abstract

Long-term potentiation (LTP) phenomenon is widely accepted as a cellular model of memory consolidation. Object recognition (OR) is a particularly useful way of studying declarative memory in rodents because it makes use of their innate preference for novel over familiar objects. In this study, mice had electrodes implanted in the hippocampal Schaffer collaterals-pyramidal CA1 pathway and were trained for OR. Field EPSPs evoked at the CA3-CA1 synapse were recorded at the moment of training and at different times thereafter. LTP-like synaptic enhancement was found 6 h posttraining. A testing session was conducted 24 h after training, in the presence of one familiar and one novel object. Hippocampal synaptic facilitation was observed during exploration of familiar and novel objects. A short depotentiation period was observed early after the test and was followed by a later phase of synaptic efficacy enhancement. Here, we show that OR memory consolidation is accompanied by transient potentiation in the hippocampal CA3-CA1 synapses, while reconsolidation of this memory requires a short-lasting phase of depotentiation that could account for its well described vulnerability. The late synaptic enhancement phase, on the other hand, would be a consequence of memory restabilization.hippocampus | long-term potentiation | memory consolidation and reconsolidation | synaptic plasticity

Interleukin-1α and HMGB1 Mediate Hippocampal Dysfunction in SIGIRR-Deficient Mice

“…The present data show that both LTP and hippocampal-dependent cognition were markedly decreased in SIGIRR Ϫ/Ϫ mice providing further evidence of the negative impact of inflammation on synaptic plasticity, and identifying a specific role for SIGIRR in maintenance of optimal cognitive and network function. Novel object recognition and Y-maze performances are known to be coupled with changes in LTP at hippocampal synapses Clarke et al, 2010). Furthermore, impaired novel object recognition, associated with inflammatory responses, has been reported in a number of experimental models including transgenic mice expressing AD pathology (Feng et al, 2004;Heneka et al, 2006;Jardanhazi-Kurutz et al, 2010) and aged animals (Pitsikas et al, 2005;Garelick et al, 2009).…”

Fear Memory

“…The typical hippocampal electroencephalographic 4 -10 Hz "theta" rhythm, which accompanies and denotes arousal or movement, is nothing but a succession of CA1 evoked potentials caused by the activation of the septo¡DG¡CA3¡CA1 pathway (216,217), which are envelopes of the corresponding CA1 cell excitatory postsynaptic potentials (EPSPs) caused by rhythmic excitatory inputs from CA3 cells in response to 4 -10 Hz bursts of medial septal cells elicited by reticular stimulation (216). Hippocampal CA1 evoked potentials are regularly used to measure LTP chronically (125,226).…”

Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation

“…Because long-term changes in synaptic efficacy in the hippocampus seems to be necessary for learning and memory (Daoudal and Debanne, 2003;Gruart et al, 2006;Clarke et al, 2010), we examined the role of PARP-1 in the long-lasting changes of synaptic transmission efficacy induced by highfrequency stimulation (HFS) at the CA3-CA1 synapses. Tiq-A administration before six HFS protocols (HFS, consisting of five trains at 200 Hz, lasting 100 ms, and presented at a rate of 1/s) provoked a deficit in long-LTP when compared with vehicleinjected mice tested 1 or 2 h after application of HFS protocol as suggested by the time ϫ treatment interaction (F (50,9) ϭ 6.19, p Ͻ 0.001; the fEPSP slope 1 h after HFS was 165.95 Ϯ 8.95 and 117.57 Ϯ 10.09 for vehicle-and Tiq-A-injected mice, respectively, and 2 h after HFS was 182.22 Ϯ 4.21 and 110.54 Ϯ 5.21 for vehicle-and Tiq-A-injected mice, respectively) ( Fig.…”