Memory Reconsolidation

Definition

Standard consolidation holds that a memory is labile shortly after encoding and then becomes fixed. Reconsolidation holds that reactivation can reopen that lability.

The window is commonly reported as several hours after a brief reminder. Within it, interference — pharmacological or behavioural — can alter what is subsequently retrieved.

The boundary conditions matter more than the phenomenon: reactivation only destabilises a memory under particular conditions, notably when the reminder generates prediction error, and old or strongly encoded memories are more resistant.

History

Reported in the 1960s, then largely abandoned. Revived by Nader, Schafe and LeDoux in 2000, who showed that a protein synthesis inhibitor in the amygdala after reactivation impaired a previously consolidated fear memory in rats.

That paper reopened a question the field had considered closed, and the human translation began soon after.

Theory

The functional argument is that reconsolidation exists to update memories: a stored memory that can never be revised is of limited use to an organism in a changing environment.

Prediction error is the trigger. A reminder that fully matches expectation does not destabilise; a reminder that violates expectation does. This connects reconsolidation directly to the learning theory behind classical conditioning, and it is the best current explanation of why reactivation sometimes opens the window and sometimes does not.

The clinical attraction is that reconsolidation-based interference would modify the original memory rather than adding inhibitory learning on top, which would avoid the return of fear that follows extinction.

Research

Animal work is robust. Human work is considerably more mixed.

Schiller and colleagues reported that extinction training delivered inside the reconsolidation window prevented the return of fear in humans. The finding attracted enormous attention and replication has been inconsistent, with several well-powered failures.

Propranolol given after reactivation has shown reductions in the expression of conditioned fear in some studies and not in others, and clinical trials in PTSD have produced mixed results.

The honest summary is that the basic phenomenon is well established in animals, the boundary conditions in humans are not well understood, and the clinical translation has not yet delivered.

Applications

Potential, not established, applications in PTSD, phobia and addiction treatment. Reconsolidation is also invoked as a mechanism in memory-focused psychotherapies, sometimes with more confidence than the evidence supports.

The forensic implication is the more secure one: retrieval is not passive, and a memory that has been questioned repeatedly is not the memory that existed before questioning.

Criticism

• Human replication is weak. The headline clinical findings have not held up consistently.
• Boundary conditions are used post hoc. When a study fails, an unmet boundary condition can always be proposed, which makes the theory hard to falsify as usually applied.
• Null results are hard to interpret: was the window not opened, or does the effect not exist?
• Clinical claims outrun the data. Several therapy models market themselves on reconsolidation with no direct evidence that it is what their procedure does.

References

• Nader, K., Schafe, G. E., & LeDoux, J. E. (2000). Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature, 406, 722-726.
• Schiller, D., et al. (2010). Preventing the return of fear in humans using reconsolidation update mechanisms. Nature, 463, 49-53.
• Kindt, M., Soeter, M., & Vervliet, B. (2009). Beyond extinction: Erasing human fear responses. Nature Neuroscience, 12, 256-258.
• Elsey, J. W. B., Van Ast, V. A., & Kindt, M. (2018). Human memory reconsolidation: A guiding framework and critical review. Psychological Bulletin, 144(8), 797-848.