Notwithstanding these promising findings, a limitation in human memory research is that the underlying neurobiological processes of memory reconsolidation can neither be directly observed nor locally targeted.
An abrupt reduction in fear responding by a single amnesic drug administered upon a very brief memory reactivation has been repeatedly demonstrated in healthy participants, and more recently in a clinical sample as well 8, 9, 10, 11, 12, 13, 14, 15, 16, 17. A single intervention that instantaneously neutralizes the emotional impact of fearful memories would signify a true paradigm shift in the practice of psychotherapy. Treatments for disorders of emotional memory generally involve multiple or prolonged sessions in which the fear gradually subsides 7. These findings have provided a strong impetus for research into whether this phenomenon of post-reactivation amnesia can be observed in humans as well 6. Post-reactivation amnesia for learned fear has now been demonstrated in a range of model organisms, from fish, to crabs, to rats 5. Gene transcription, RNA translation, and protein synthesis are necessary for reconsolidation and these neurobiological processes enable to fundamentally change a fear memory engram 2, 5. It refers to the idea that reactivation can induce a transient, labile state in a previously stable memory, during which the memory is sensitive to disruption or modification, necessitating a time-dependent process of restablization in order to persist. Observations of post-reactivation amnesia for learned fear have drastically changed the neuroscience literature on memory by generating a novel and influential conceptual framework, known as memory reconsolidation 1, 2, 3, 4, 5.
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