Reminder effects: the molecular cascade following a reminder in young chicks does not recapitulate that following training on a passive avoidance task

Abstract

Memory traces, once established, are no longer sensitive to disruption by metabolic inhibitors. However, memories reactivated by reminder are once again vulnerable, in a time-dependent manner, to amnestic treatment. To determine whether the metabolic events following a reminder recapitulate those following initial training we examined the temporal dynamics of amnesia induced by the protein synthesis inhibitor anisomycin and the glycosylation inhibitor 2-deoxygalactose. The effects of both were transient and dependent on time of reminder post-training and time of injection relative to reminder, and differed from those following initial training. 2-[(14)C]-deoxyglucose uptake increased in two brain regions, the intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO) following reminder as it did following training, but the increase was bilateral rather than confined to the left hemisphere and was more marked in LPO than IMHV. C-fos expression after reminder was increased only in the LPO, the chick brain region associated with a late phase of memory processing and recall. Thus although, like initial consolidation, memory processing after reminder is sensitive to inhibitors of protein synthesis and glycosylation, the temporal and pharmacological dynamics indicate differences between these two processes.

Activation of the transcription factor NF-κB by retrieval is required for long-term memory reconsolidation

“…Following memory reactivation, neurotransmitter antagonists and metabolic inhibitors have shown effective doses and time windows different from those observed for initial consolidation. In some cases, the effect in reconsolidation was only transient and/or required different neuronal substrates (Summers et al 1997;Przybyslawski et al 1999;Bahar et al 2004;Salinska et al 2004). The inhibition in hippocampus of the TF C/EBP in Figure 5.…”

“…Whether such a memory phase, termed reconsolidation, is mechanistically similar to the initial consolidation is a matter of debate (Debiec et al 2002;Myers and Davis 2002;Lee et al 2004;Salinska et al 2004). Little is known about the molecular pathways involved in this process.…”

Characterization of Fear Memory Reconsolidation

“…Given that Vianna et al (2001) did not test for PR-STM, then it is not clear that the reported deficit is related to reconsolidation. The majority of studies that have tested for recovery and reported intact PR-STM and impaired PR-LTM have not found recovery from amnesia (Debiec et al, 2002;Bozon et al, 2003;Child et al, 2003;Pedreira and Maldonado, 2003;Suzuki et al, 2004), whereas one group has reported recovery in newborn chicks (Anokhin et al, 2002;Salinska et al, 2004). Thus, at this point, there is little modern evidence for spontaneous recovery from a specific impairment in reconsolidation.…”

The role of protein synthesis during the labile phases of memory: Revisiting the skepticism

“…Anokhin, Tiunova, & Rose, 2002;Lattal & Abel, 2004;Power, Berlau, McGaugh, & Steward, 2006;Riccio, Moody, & Millin, 2002;Riccio. Millin, & Bogart, 2006;Salinska, Bourne, & Rose, 2004). However, opposite results have been reported in other cases, in which the memory deficits observed after the administration of protein synthesis inhibitors were persistent (e.g.…”