Abstract

Existing memories, when retrieved under certain circumstances, can undergo modification through the protein synthesis-dependent process of reconsolidation. Disruption of this process can lead to the weakening of a memory trace, an approach which is being examined as a potential treatment for disorders characterized by pathological memories, such as Post-Traumatic Stress Disorder. The success of this approach relies upon the ability to robustly attenuate reconsolidation; however, the available literature brings into question the reliability of the various drugs used to achieve such a blockade. The identification of a drug or intervention that can reliably disrupt reconsolidation without requiring intracranial access for administration would be extremely useful. Electroconvulsive shock (ECS) delivered after memory retrieval has been demonstrated in some studies to disrupt memory reconsolidation; however, there exists a paucity of literature characterizing its effects on Pavlovian fear memory. Considering this, we chose to examine ECS as an inexpensive and facile means to impair reconsolidation in rats. Here we show that electroconvulsive seizure induction, when administered after memory retrieval, (immediately, after 30 min, or after 1 h), does not impair the reconsolidation of cued or contextual Pavlovian fear memories. On the contrary, ECS administration immediately after extinction training may modestly impair the consolidation of fear extinction memory.

Highlights

  • Retrieved memories can undergo updating or modification under certain circumstances

  • The following day, the animals were returned to the testing context for a post-reactivation long-term memory (PR-LTM) test to determine the effects of Electroconvulsive shock (ECS) on memory persistence (Figure 1c,f)

  • We observed an inflation of memory strength resulting from the immediate administration of ECS after contextual reactivation when measured at PR-LTM, (Figure 2)

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Summary

Introduction

Retrieved memories can undergo updating or modification under certain circumstances. The retrieval of a memory can cause the memory engram neurons to undergo another bout of plasticity, which can weaken or strengthen the memory through synapse reorganization [5,6,7,8]. If a protein synthesis inhibitor is administered immediately after memory retrieval, the reconsolidation process can be inhibited, weakening the memory. This phenomenon has been shown to occur across multiple memory types and documented using a variety of species [9,10,11,12,13]. There is a plethora of information available on the subject curated by labs across the globe, and many believe this process has the potential to be harnessed as a treatment for disorders characterized by maladaptive memories, such as anxiety disorders and drug addiction [14,15,16,17]

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