The terms consolidation and reconsolidation refer to transient neurobiological processes that are thought to implement changes in synaptic efficacy in neurons that participate in forming a memory, thereby over time stabilizing the memory and rendering it relatively permanent (or long-term). Consolidation follows initial memory acquisition, whereas reconsolidation follows reactivation of a memory that already has been consolidated, as during memory recall or retrieval.
Although most researchers studying the neuroscience of memory have embraced the concept of memory consolidation, reconsolidation was initially met with strong skepticism. The idea that long-term memory, regardless of its remoteness, can enter states of plasticity after reactivation, similar to the states observed shortly after acquisition, challenges the consolidation model, which proposes an irreversible memory-stabilization process that fixes memory permanently.
The concept that both consolidation and reconsolidation exist as time-dependent stabilization processes is deduced from structurally equivalent data sets by applying identical operant definitions and basic assumptions. These data sets show that amnesic treatments can affect memory only when they are applied shortly after memory acquisition (consolidation) or reactivation (reconsolidation), and that there is intact short-term but impaired long-term memory following the amnesic treatment.
Alternative explanations for the memory impairment that follows post-reactivation amnesic treatment have been proposed (for example, that the cause is treatment-induced lesions, transient retrieval blockade, facilitated extinction or new learning), but none of these interpretations can explain all of the available reactivation-induced memory-instability data (unlike the reconsolidation hypothesis itself). Furthermore, as reconsolidation and consolidation are deduced from very similar data sets using identical operant definitions, these interpretations also fall short of fully explaining results from consolidation studies.
Some argue that the existence of boundary conditions that moderate the occurrence of reconsolidation processes limits the validity rather than informing about the nature of reconsolidation. Therefore the criticism — based on the terminology — that reconsolidation should exactly recapitulate consolidation and occur for each and every memory is not justified.
The existing consolidation framework cannot accommodate the reconsolidation data. A new neurobiological model of memory is needed that acknowledges the long-held notion prominent in cognitive psychology that memory, at any age, is in essence plastic.
Consolidated memories can re-enter states of transient instability following reactivation, from which they must again stabilize in order to persist, contradicting the previously dominant view that memory and its associated plasticity mechanisms progressively and irreversibly decline with time. We witness exciting times, as neuroscience begins embracing a position, long-held in cognitive psychology, that recognizes memory as a principally dynamic process. In light of remaining controversy, we here establish that the same operational definitions and types of evidence underpin the deduction of both reconsolidation and consolidation, thus validating the extrapolation that post-retrieval memory plasticity reflects processes akin to those that stabilized the memory following acquisition.
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K.N. was supported by the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council of Canada, the Canadian Foundation for Innovation and the Volkswagen, Alfred P. Sloan and EJLB Foundations; K.N. is a William Dawson chair and a E.W.R. Steacie Memorial Fellow; O.H. is supported by the Deutsche Forschungsgemeinschaft. We would like to thank the Fondation des Treilles for hosting us while we wrote this manuscript. We thank C. Rankin, P. Frankland, E. Balaban and J. LeDoux for their comments on this manuscript.
- Fear conditioning
A Pavlovian conditioning paradigm in which an initially neutral stimulus (for example, a tone or the context in which the animals are conditioned) is paired with another stimulus that evokes pain or strong somatic discomfort (typically a footshock). After a single pairing the initially neutral stimulus will elicit a spectrum of fear-like or defensive responses.
- Short-term memory
(STM). Transient memory for an experience that does not require synthesis of new proteins or RNA and that can be expressed immediately. Typically, STM duration ranges from immediately to a couple of hours after acquisition.
- Long-term memory
(LTM). Relatively stable memory that develops over time and is assumed to be mediated by changes in synaptic efficacy. LTM depends on synthesis of new proteins and RNA. Typically it is tested one or more days after training, as it takes several hours to stabilize. Once stabilized it can last for the remainder of the animal's life.
- Long-term potentiation
(LTP). Traditionally demonstrated in hippocampal slice preparations, LTP is a persistent (lasting hours to days) enhancement of synaptic efficacy. It is rapidly induced by short high-frequency (tetanic) stimulation of a synaptic pathway.
- Long-term depression
(LTD). A persistent reduction of synaptic efficacy that can be induced by repeated low-frequency stimulation of a synaptic pathway. Maintenance of LTD might require de novo protein synthesis.
- Post-reactivation short-term memory
(PR-STM). By analogy with STM, PR-STM refers to a transient state into which existing LTM enters after it has been reactivated. The initial studies on reconsolidation indicate that PR-STM does not require synthesis of new RNA or proteins.
- Post-reactivation long-term memory
(PR-LTM). By analogy with LTM, PR-LTM refers to the period of stability that reactivated memory enters after completing reconsolidation.
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Nader, K., Hardt, O. A single standard for memory: the case for reconsolidation. Nat Rev Neurosci 10, 224–234 (2009). https://doi.org/10.1038/nrn2590
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