Abstract

We recently proposed that retrograde amnesia does not result from a disruption of the consolidation/reconsolidation processes but rather to the integration of the internal state induced by the amnesic treatment within the initial memory. Accordingly, the performance disruption induced by an amnesic agent does not result from a disruption of the memory fixation process, but from a difference in the internal state present during the learning phase (or reactivation) and at the later retention test: a case of state-dependency. In the present article, we will review similarities and differences these two competing views may have on memory processing. We will also consider the consequences the integration concept may have on the way memory is built, maintained and retrieved, as well as future research perspectives that such a new view may generate.

Highlights

  • We recently proposed that retrograde amnesia does not result from a disruption of the consolidation/reconsolidation processes but rather to the integration of the internal state induced by the amnesic treatment within the initial memory

  • In a recent study we showed that the administration of cycloheximide, a protein synthesis inhibitor, or of lithium chloride, a substance inducing strong nausea, delivered just after the reactivation of an inhibitory avoidance memory, induced a strong performance disruption, which was abolished by delivering again the same treatment before the retention test (Gisquet-Verrier et al, 2015)

  • Unlike the consolidation hypothesis which analyses retrograde amnesia and facilitative effects as resulting from two opposite causes, namely disrupting or enhancing the consolidation process, we propose that both effects result from the same process: the integration of a new information within the memory which leads to two opposite outcomes

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Summary

Original Findings and Interpretation

There have been hundreds of publications describing the findings that treatments delivered after training or after the reactivation of a memory disrupt the retention performance. Memory Integration previously developed by Müller and Pilzecker (1900) whose work on retroactive interference led them to suggest that new memories are fragile, requiring time to undergo a consolidation phase before being fixed Disrupting this process by treatments interfering with the normal brain functioning was supposed to prevent memory formation and to lead to amnesia. The other would be an inactive form, typical of stored but potentially accessible memories, that would not be affected by any amnesic treatments Another finding, published around the same time, indicated that the disruption of performance was not detectable during the first few hours, but occurred only later (Geller et al, 1970; Miller and Springer, 1971, 1972; Hinderliter et al, 1975).

An Alternative Interpretation
Current Views on the Consolidation Hypothesis
How State Dependency Can Explain Delayed Onset of Retrograde Amnesia
How State Dependency Can Explain Recovery of Amnesia
Relationship of Certain Training Conditions to State Dependency
THE CONCEPT OF MEMORY INTEGRATION
Case of Facilitative Treatments
Memory Interference
Boundary Conditions
Malleability of Active Memory
Processing of New Information
Memory Is Not Erased but Can Be Modified
Do Memories Require New Protein Synthesis?
Neuronal Networks May Not Constitute the Support of Memory Traces
Memories Are Rapidly Formed and Can Be Rapidly Modified
State at the Time of Testing Determines Retrieval
Memory Integration for New Therapeutic Approaches
CONSEQUENCES AND PERSPECTIVE
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