HIGHLIGHTSReconsolidation—memory malleability after retrieval—does not occur invariably.Several factors affect a memory’s sensitivity to destabilization after retrieval.Experience‐driven changes in synaptic plasticity processes resemble metaplasticity.NMDAR receptors initiate bidirectional plasticity and also memory… Click to show full abstract
HIGHLIGHTSReconsolidation—memory malleability after retrieval—does not occur invariably.Several factors affect a memory’s sensitivity to destabilization after retrieval.Experience‐driven changes in synaptic plasticity processes resemble metaplasticity.NMDAR receptors initiate bidirectional plasticity and also memory destabilization.The ratio of GluN2A:GluN2B NMDAR subunits may contribute to memory stability. ABSTRACT Reconsolidation, a process by which long‐term memories are rendered malleable following retrieval, has been shown to occur across many different species and types of memory. However, there are conditions under which memories do not reconsolidate, and the reasons for this are poorly understood. One emerging theory is that these boundary conditions are mediated by a form of metaplasticity: cellular changes through which experience can affect future synaptic plasticity. We review evidence that N‐methyl‐D‐aspartate receptors (NMDARs) might contribute to this phenomenon, and hypothesize that resistance to memory destabilization may be mediated by the ratio of GluN2A/GluN2B subunits that make up these receptors. Qualities such as memory strength and the age of the memory may increase the GluN2A/GluN2B ratio, reducing the ability of reactivation cues to induce destabilization, thereby preventing reconsolidation. Other examples of experience‐dependent learning and evolutionary perspectives of reconsolidation are also discussed.
               
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