Mechanisms of memory consolidation: The effect of reminder

Mileusnic, Radmila; Lancashire, Christine and Rose, Steven (2006). Mechanisms of memory consolidation: The effect of reminder. In: Ruzdijic, Sabera and Rakic, Ljubisa eds. Neurobiological studies - From genes to behaviour. Kerala, India: Research Signpost, pp. 71–84.

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Abstract

The translation of a short-term into longer term memory (consolidation) requires protein synthesis, presumed to be necessary for the resculpting of synapses. Inhibitors of protein synthesis, administered around the time of training or 4-6 hours later produce lasting amnesia for the task. Beyond this time, the memory is insensitive to the inhibitors of protein synthesis, and has been regarded as permanent. However, as older observations, recently reconfirmed, show, reminding the animal of the previously learned experience renders the memory labile once more. Administration of protein synthesis inhibitors in association with the reminder for an aversive experience produces amnesia for the task, in some cases apparently permanent, in others more transient. Thus, the pharmacological lability of memory following a reminder is far from universal. This has prompted an ongoing debate: is the amnesia due to a blockade of the same biochemical cascade as is involved in the initial consolidation (hence permanently preventing ‘reconsolidation’) or does it represents a temporary failure to access the memory (retrieval). This distinction is in some cases artificial, as any reminder inevitably constitutes a new experience, and will involve some learning, which may be part of a process leading to extinction of the earlier memory. A further complexity is added by the fact that even without reminder, putative memory traces are not entirely stable, migrating from one brain region to others over a period that may vary from hours to weeks.

Our laboratory been studying these phenomena using a one trial passive avoidance task in young chicks, and the effects of the anisomycin and colchicine on recall following both training and reminder. Results obtained require us to reconsider the nature of the biochemical processes initiated by the reminder, suggesting as they do that reminder engage local synaptic and dendritic processes, not necessarily in the same cells or brain regions as those involved in initial consolidation. This distinction may account for the transient nature of the amnesia produced by protein synthesis inhibitors following a reminder.

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