Linking New Information to a Reactivated Memory Requires Consolidation and Not Reconsolidation Mechanisms

Abstract

A new memory is initially labile and becomes stabilized through a process of consolidation, which depends on gene expression. Stable memories, however, can again become labile if reactivated by recall and require another phase of protein synthesis in order to be maintained. This process is known as reconsolidation. The functional significance of the labile phase of reconsolidation is unknown; one hypothesis proposes that it is required to link new information with reactivated memories. Reconsolidation is distinct from the initial consolidation, and one distinction is that the requirement for specific proteins or general protein synthesis during the two processes occurs in different brain areas. Here, we identified an anatomically distinctive molecular requirement that doubly dissociates consolidation from reconsolidation of an inhibitory avoidance memory. We then used this requirement to investigate whether reconsolidation and consolidation are involved in linking new information with reactivated memories. In contrast to what the hypothesis predicted, we found that reconsolidation does not contribute to the formation of an association between new and reactivated information. Instead, it recruits mechanisms similar to those underlying consolidation of a new memory. Thus, linking new information to a reactivated memory is mediated by consolidation and not reconsolidation mechanisms.

The temporal dynamics of consolidation and reconsolidation decrease during postnatal development

“…However, by using the same dose of AN in the same task, we can have an indication of the duration of this crucial stage for long-term memory formation. With respect to this stage, the durations of consolidation and reconsolidation evolve in parallel during development; in the adult, similarities and differences between them are still being explored (Dudai 2004;Alberini 2005;Tronel et al 2005;Davis and Laroche 2006;Sara and Hars 2006;Tronson and Taylor 2007). The parallelism observed here during postnatal development suggests that both involve some common processes.…”

“…Considering the very short period during which the AN was effective at the end of nursing, we tested the effect of AN at a dose of 210 mg/kg, the highest dose generally used in the adult (Davis et al 1980;Tronel et al 2005), in post-weaning rats at the age of P35. The animals were autonomous, so they were submitted to a conventional paradigm of conditioned taste aversion where they were allowed to drink aromatized water (CS) from pipettes and 30 min later poisoned (US) by LiCl injection.…”

“…(42 mg/kg or 210 mg/kg in the last experiment) after training or reactivation. The dose of 42 mg/kg was previously shown to be effective in producing a total amnesia in P3 pup (Gruest et al 2004b) and the dose of 210 mg/kg is the upper one commonly used in adult rodent (Davis et al 1980;Tronel et al 2005). Control rats were injected with 0.9% saline.…”

Activation of Hippocampal Nuclear Factor-κB by Retrieval Is Required for Memory Reconsolidation

“…On the one hand, data support hippocampal involvement in both consolidation and reconsolidation (Debiec et al, 2002;Rossato et al, 2006), and, in contrast, data support that hippocampus is involved in consolidation but not in reconsolidation (Taubenfeld et al, 2001;Tronel et al, 2005).…”

Characterization of spatial memory reconsolidation

“…Thus, one main function of reconsolidation is considered to be memory updating (Pedreira et al 2004;Rossato et al 2006). Even though Tronel et al (2005) concluded that reconsolidation was not required to link new information to a retrieved memory, Lee (2008) demonstrated that an adaptive function of the reconsolidation process enables the update of memory's content. Without the presence of new information, thus when updating is not necessary, a very well-learned memory does not undergo reconsolidation (Rodriguez-Ortiz et al 2005;Winters et al 2009).…”