Process consolidating memories
Additional corroboration of the same phenomenon was provided by Suzuki et al.
 who, using systemic anisomycin injections in mice at time points covering an 8-week temporal window after training, elegantly showed that contextual fear conditioning displays a gradient of postreactivation fragility.
Disrupting events include brain trauma, seizure, electroconvulsive shock (ECS), brain cooling, new learning, and the administration of drugs such as inhibitors of protein and RNA synthesis.
In conflict with this view, recent results, extending earlier observations, show that after reaching a “stable” state, memory can become transiently labile again if reactivated, for example, by recall .
It seems reasonable to believe that, indeed, different interfering manipulations target different phases or perhaps different stages of memory consolidation.
In fact, the same memory would be considered consolidated in studies that use protein synthesis inhibitors, but still unconsolidated in investigations that assess, for example, its hippocampal dependence.
The dissociation between the effects of systemically and centrally administered anisomycin on remote memory led the authors to suggest that memory stability is due, in part, to the distributed nature of remote contextual fear memory traces.Based on this, I would like to argue that the reconsolidation phenomenon reflects a fragile state of a memory that has not yet been fully consolidated, although it has passed the initial protein synthesis-dependent phase.
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