Abstract
Reconsolidation of memories has mostly been studied at the behavioral and molecular level. Here, we put forward a simple extension of existing computational models of synaptic consolidation to capture hippocampal slice experiments that have been interpreted as reconsolidation at the synaptic level. The model implements reconsolidation through stabilization of consolidated synapses by stabilizing entities combined with an activity-dependent reservoir of stabilizing entities that are immune to protein synthesis inhibition (PSI). We derive a reduced version of our model to explore the conditions under which synaptic reconsolidation does or does not occur, often referred to as the boundary conditions of reconsolidation. We find that our computational model of synaptic reconsolidation displays complex boundary conditions. Our results suggest that a limited resource of hypothetical stabilizing molecules or complexes, which may be implemented by protein phosphorylation or different receptor subtypes, can underlie the phenomenon of synaptic reconsolidation.
Highlights
Reconsolidation describes a process for the alteration of memories, and highlights the dynamic nature of information processing and storage in the brain
We found two necessary features: stabilization of consolidated synapses, and an activity-dependent reservoir of stabilizing entities that is immune to protein synthesis inhibition (PSI)
Our model implements, using simple kinetics, two key features of slice-based reconsolidation: stabilization of consolidated synapses through the binding of stabilizing entities (Figure 2A), and an activity dependent reservoir of synaptic stabilizing entities that is immune to PSI (Figures 1B, 2B)
Summary
Reconsolidation describes a process for the alteration of memories, and highlights the dynamic nature of information processing and storage in the brain. Reconsolidation represents the phenomenon that recently triggered memories are susceptible to degradation whereas memories that have not been retrieved are spared from degradation (Nader et al, 2000). Scant evidence exists as to the nature of the circuit and cellular level phenomenon of reconsolidation, as opposed to the phenomenon of consolidationāthe initial storage of a memoryāfor which a vast literature exists based on slice electrophysiology (Redondo and Morris, 2011). Recent reviews (Nader and Hardt, 2009; Besnard et al, 2012) have highlighted the potential link of behavioral reconsolidation to experiments on long-term potentiation (LTP) in hippocampal slices. To make that link they cited an elegant set of experiments (Fonseca et al, 2006a) that caused the degradation of potentiated synapses through the interaction of stimulation and PSI
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