consolidation hypothesis psychology definition

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What Is Memory Consolidation?

Connecting new information to long-term memories

Kendra Cherry, MS, is a psychosocial rehabilitation specialist, psychology educator, and author of the "Everything Psychology Book."

consolidation hypothesis psychology definition

Sean is a fact-checker and researcher with experience in sociology, field research, and data analytics.

Tara Moore / Getty Images

Building Long-Term Memories With New Information

How memory consolidation works, influences on memory consolidation, speeding up memory consolidation.

Short-term memory tends to be limited in duration and capacity. In fact, the human brain can store short-term memories for only about 30 seconds—so it must move important information into long-term memory to retain it. That's where memory consolidation comes in.

Memory consolidation is the process in the brain that converts short-term memories into long-term ones.

Memory consolidation relies on synapses in the brain. In something akin to an electrical system conducting a current,r the synapses pass signals from neuron to neuron with the help of neurotransmitters.

The more frequently signals are passed, the stronger the synapses become. This process, called potentiation, is believed to play a major role in learning and memory processes.

When two neurons fire at the same time repeatedly, they become more likely to fire together in the future. Eventually, these two neurons become sensitized to one another.

As you acquire new experiences and memories, your brain creates more and more of these connections. Essentially, the brain rearranges itself, establishing new connections while weeding out old ones.

By rehearsing or recalling information repeatedly, these neural networks strengthen. For example, if you study the same material regularly over a long period, the pathways involved in remembering that information become stronger. The repeated firing of the same neurons makes it more likely that those same neurons will be able to repeat that firing in the future. As a result, you'll remember the information later with ease and accuracy.

Here's another way to think of these synaptic pathways: They're similar to a path in the woods. The more often you walk the path, the more familiar it becomes and the easier it is to traverse .

Although we often think of the brain as a filing cabinet or a computer with individual files of memories carefully stored away, the reality is that memories are spread out across the entire brain.

Through the consolidation process, the brain creates a sort of neural map, allowing memories to be retrieved when needed.

Sleep can play an important role in the consolidation process. One of the major theories of sleep suggests that it's a way to process and consolidate information we acquire during our waking lives.

People often think of memories as permanent, but just because a memory has been consolidated does not mean you can't lose it. Researchers have found that memories often need to be reconsolidated once they have been recalled. The process of recalling and reconsolidating a memory can help maintain and strengthen information in long-term memory.

Researchers have also found that memories must be reconsolidated every time you access them. This process, however, can transform and change the memory itself. The very act of remembering, it seems, can lead to some things being forgotten.

It is also possible to speed up the consolidation process when learning new information. Rehearsal and memorization strategies, such as using mnemonic devices and studying are a few techniques. One of the best ways to ensure that information is consolidated into long-term memory is to rehearse it over several spaced intervals repeatedly.

That's why going over your class notes once a week for several weeks will lead to greater memory retention than cramming the night before an exam.

A Word From Verywell

By understanding how consolidation works, you might be able to adapt your memorization strategies to boost the process. Repetition/study and sleep are good places to start.

Himmer, L., Schönauer, M., Heib, D. P. J., Schabus, M., & Gais, S. (2019). Rehearsal initiates systems memory consolidation, sleep makes it last . Science Advances , 5 (4), eaav1695. doi:10.1126/sciadv.aav1695

Rasch B, Born J. About sleep's role in memory . Physiol Rev . 2013;93(2):681-766. doi: 10.1152/physrev.00032.2012

Alberini CM, Ledoux JE. Memory reconsolidation . Curr Biol . 2013;23(17):R746-50. doi: 10.1016/j.cub.2013.06.046

Milner B, Corkin S, Teuber HL. Further analysis of the hippocampal amnesic syndrome: 14-year follow-up study of H.M . Neuropsychologia. 1968;6(3):215. doi:10.1016/0028-3932(68)90021-3

Payne J.D, Kensinger EA. Sleep’s role in the consolidation of emotional episodic memories . Current Directions in Psychological Science. 2010;19(5):290-295. doi:10.1177/0963721410383978

By Kendra Cherry, MSEd Kendra Cherry, MS, is a psychosocial rehabilitation specialist, psychology educator, and author of the "Everything Psychology Book."

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Memory--a century of consolidation

Affiliation.

1 the Center for the Neurobiology of Learning and Memory and the Department of Neurobiology and Behavior, University of California Irvine, Irvine, CA 92697, USA. [email protected]
PMID: 10634773
DOI: 10.1126/science.287.5451.248

The memory consolidation hypothesis proposed 100 years ago by Müller and Pilzecker continues to guide memory research. The hypothesis that new memories consolidate slowly over time has stimulated studies revealing the hormonal and neural influences regulating memory consolidation, as well as molecular and cellular mechanisms. This review examines the progress made over the century in understanding the time-dependent processes that create our lasting memories.

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100 Years of Consolidation— Remembering Müller and Pilzecker

Hilde A. Lechner 1 ,
Larry R. Squire 2 , and
John H. Byrne
1 W.M. Keck Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Anatomy, University of Texas–Houston Medical School, Houston, Texas 77030 USA, 2 Veterans Affairs Medical Center, San Diego, and Departments of Psychiatry, Neurosciences, and Psychology, University of California, San Diego, La Jolla, California 92093 USA

The origin of the concept of memory consolidation and the introduction of the term “consolidirung” (consolidation) to the modern science of memory are generally credited to Georg Elias Müller (1850–1934), professor at the University of Göttingen, Germany, and his student Alfons Pilzecker. Their seminal monograph “Experimentelle Beiträge zur Lehre vom Gedächtnis” (Experimental Contributions to the Science of Memory), published in 1900, proposed that learning does not induce instantaneous, permanent memories but that memory takes time to be fixed (or consolidated). Consequently, memory remains vulnerable to disruption for a period of time after learning.

Georg Müller was among the founders of experimental psychology. Inspired by the work of Gustav Fechner (1801–1887), Wilhelm Wundt (1832–1920), and Herman Ebbinghaus (1859–1909), 5 he was an early advocate of the view that mental function results from the action of matter, and that learning and memory should thus exhibit lawful properties. In their 300-page monograph, Müller and Pilzecker reported 40 experiments, carried out between 1892 and 1900, which were designed to identify the laws that govern memory formation and retrieval. Although Müller and Pilzecker have been frequently acknowledged for introducing the concept of memory consolidation, 2 their monograph has not been translated and knowledge of their methods and experimental findings has faded with the passing of almost a century. This commentary is intended to outline the experimental work of Müller and Pilzecker to explicate how the concept of memory consolidation originated. 3

In their studies, Müller and Pilzecker used lists of nonsense syllables, which had been introduced by Ebbinghaus (1885) . In his experiments, Ebbinghaus determined the number of trials that were needed to reproduce all of the syllables in a studied list twice without error (method of complete mastery). The methods of Müller and Pilzecker differed in three ways. First, they trained their subjects using nonsense syllables that were presented as paired associates. Lists were read aloud with emphasis on every odd-numbered syllable, thus creating pairs of emphasized and nonemphasized syllables, or trochees. To test memory, volunteers were cued with the first syllable of each pair, in a mixed order, and asked to recall the second syllable of the pair. Thus, if the list A-b-C-d-E-f were used for training (where each uppercase letter denotes the emphasized syllable of a pair), the correct answers to the cue syllables E, A, C would be the syllables f, b, and d. This novel procedure had originally been developed in Müller’s laboratory by Jost (1897) . Second, instead of counting the number of trials necessary to reproduce the paired associates correctly, Müller and Pilzecker fixed the number of training trials and quantified memory by determining the percentage of correctly recalled syllables, the percentage of incorrect answers, and the percentage of recall failures. This method is in such common use today that it is not often appreciated as an experimental innovation. Third, they constructed a sophisticated apparatus for determining the response latency for recall (see for details).

The Beginnings of Consolidation Theory

The line of evidence that would eventually result in the concept of memory consolidation began with a simple observation. Volunteers for the experiments of Müller and Pilzecker occasionally reported a strong tendency for syllable pairs to come to mind repeatedly between training sessions, despite efforts to suppress this intrusion. Müller and Pilzecker adopted the German word “perseveration” (p. 60) from descriptions of psychiatric illness to refer to this benign phenomenon. Pursuing the reports of their volunteers, they found evidence for perseveration during recall testing itself. For example, some individuals, recalled a syllable correctly in response to its proper cue but, in subsequent tests, continued to use the same syllable incorrectly in response to another cue (experiment 26). Also, incorrectly recalled syllables often belonged to the list that contained the correct syllable rather than being simply unrelated to previously trained material. This effect was strongest immediately after training, decayed during the subsequent minutes, and was not present after 1 day (Fig. 1 ; experiments 5, 7, 15, and 29). Müller and Pilzecker concluded that these peculiar mistakes resulted from the perseveration of recently learned material. Moreover, they speculated that perseveration was the result of transient activity in the brain that encoded the associative memory and suggested that this activity functioned as a short-term form of memory, similar to the primary memory proposed by William James (1842–1910). The sequence of our thoughts … is often interrupted by external or internal disruptions. Were it not for a spontaneous tendency of these thoughts to regain conscious awareness after a perturbation, such disturbances would prevent the completion of important trains of thought. (p. 75)

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Evidence for perseveration. Subjects were tested for retention of paired syllables at various intervals after learning by cueing them with the first syllable of each pair. Incorrect answers were divided into syllables that belonged to the same list as the cue syllable (list correct errors) and syllables that did not belong to the studied list. Plotted here is a subset of list correct errors, in which the incorrectly recalled syllable belonged to the cue of the immediately preceding pair in the study list. The percentage of these errors decreased rapidly for ∼10 min following learning. This observation was interpreted as evidence for the perseveration of the studied syllables for ∼10 min. (From data reported on p. 65; experiments 5, 7, 15, and 29).

Importantly, Müller and Pilzecker suggested that the perseveration of syllable pairs might be necessary not only for establishing representations of the syllables in memory but for strengthening the associations between them. If so, they argued, disrupting perseveration should interfere with the formation of associative learning. The experience of everyday life shows that perseverative tendencies of different parts of a train of thought can be weakened considerably by turning one’s attention with energy to a different matter. … One can question, however, whether the effect of such an intense mental occupation … , immediately following reading of a list, simply reduces the frequency with which syllables of this list spontaneously regain conscious awareness. One might deem that the perseverative tendencies of syllables of a previously read list might also serve to consolidate the associations between these syllables … and that accordingly, weakening of the perseverative tendencies of syllables from a previously read list, due to other intense mental occupations, might have the additional effect of obstructing the associations between these syllables. (p. 68)

The Discovery of Retroactive Inhibition

Müller and Pilzecker designed 10 experiments to test the hypothesis that perseveration reflected an internal, physiological process that serves to strengthen associative memories. Three representative experiments are described here. In experiment 31 (Fig. 2 ), a volunteer received eight training trials with six pairs of syllables (list A), which took ∼1 min. After an interval of 34 sec a second list (list X) was read eight times to prevent the perseveration of syllables from list A. Then, after a longer interval of 6 min, cue syllables from both lists A and X were presented in mixed order, and the percentage of correctly recalled syllables from list A was determined. To examine the effect of the interpolation of list X on recall of list A, a third list (list B) was trained eight times and recall was tested after an equivalent interval, but without interpolated learning. Retention of associations from list A was lower than retention from list B (23% vs. 48%), suggesting that the interpolation of list X had interfered with memory for the associations from list A. Similar results were obtained when the interval between list A and X was 1 min, and the retention interval was 24 hr. Müller and Pilzecker commented: The suspicion imposed on us by these results was that the processes that serve the formation of associations in a list of syllables continue for some time after reading of the list, but that they would be weakened by another intense mental occupation, such that an intense mental occupation following reading of a list of syllables would inhibit associations of that list. Because this type of inhibition acts on the effect of an ostensibly completed process … we will call it … “retroactive inhibition.” (p. 179)

Retroactive inhibition of verbal material. Lists of 12 syllables were mounted on rotating drums and read aloud as pairs by emphasizing every other syllable. A subject was given eight training trials with syllable pairs from list A (total training time, ∼1 min) followed by eight training trials with an interpolated list X. Retention was then tested 6 min after studying list X and compared to retention of a third list B, which was tested without an interfering list. Retention of list A was poorer than retention of list B, suggesting a retroactive inhibition of list X on the associations from list A. (From data reported on p. 181; experiment 31).

In another study (experiment 34), Müller and Pilzecker determined that retention (measured at 1.5 hr) of the first of two lists was impaired if the second list followed after a brief interval of 17 sec but was not affected when the second list followed after a longer interval of 6 min. This experiment suggested … that the associations of a [list] of syllables are being inhibited less by a subsequently read list, the later the [interpolated list] is being read. [This is] because the longer the interval between the first and second list, the more those processes that induce and strengthen the associations of the first list will have subsided at the time when the second list is being read and accordingly, the lesser … will be the disrupting effect of reading the second list upon these processes. (p. 184)

Retroactive Inhibition by Unrelated Material

To complete their examination of retroactive inhibition, Müller and Pilzecker asked whether the material used to suppress perseveration had to be similar to the learned material (experiment 35). To answer this question, list A was read eight times and immediately followed by the sequential presentation of three pictures showing landscapes (Fig. 3 ). Subjects were asked to describe each picture for a total of 6 min, after which retention for list A was tested. A control list (list B) was tested for retention after 6 min without intermittent distraction. Again, retention of list A was lower than retention of list B (24% vs. 56%), suggesting that mental activity unrelated to the learned material itself could be disruptive.

Retroactive inhibition by pictorial material. Syllables from list A were trained and followed immediately by a 6-min presentation of three painted landscapes. The subject was asked to describe the pictures. Retention of list A was then compared to retention of a control list B. The result suggested that even material not related to what had been studied could interfere with retention. (From data reported on p. 188; experiment 35).

Summarizing these results, Müller and Pilzecker reached the following conclusion: After all this, there is no alternative but to assume that after reading a list of syllables certain physiological processes, which serve to strengthen the associations induced during reading of that list, continue with decreasing intensity for a period of time. These processes and their facilitating effects on these associations are being weakened to a greater or lesser extent if the experimental subject experiences further mental exertion immediately after reading a list. …

It seems justified to suppose that the physiological processes mentioned here are the same that underlie perseverative tendencies. . . . . Mental exertion in an experimental subject after reading a list of syllables has firstly the direct effect of weakening the perseverative tendencies of these syllables and secondly, because the effect of these perseverative tendencies is to consolidate syllable associations, the additional effect of impairing these associations. It is the same, quickly fading perseverative tendency that is responsible for the fact that, within about 10 minutes after reading a list of syllables, the recall latency is shorter the earlier testing is done; and the impairment of [the perseverative tendency] … handicaps the associations of a list of syllables within the first 10 minutes of reading the list (pp. 196–197).

This conclusion implies that memory is consolidated with a time course of ∼10 min. Yet it should be noted that the longest interval between original learning and interpolated activity that Müller and Pilzecker studied was 6 min and that retroactive inhibition was not detected at intervals longer than 1 min. Müller and Pilzecker’s value of 10 min seems to have been an estimate drawn from the observed time course of perseveration (see Fig. 1 ).

McDougall (1901) and Burnham (1903) immediately recognized that perseveration theory provided a way to understand the temporally graded retrograde amnesia (i.e., the loss of premorbid memory) that results from traumatic head injury. Systematic laboratory studies of retrograde amnesia using electroconvulsive shock (ECS) in rats were pioneered by Carl Duncan and generally supported the estimates of Müller and Pilzecker for the time course of consolidation. In these experiments, temporally graded retrograde amnesia for an active avoidance task was produced by ECS up to 15 min following learning but not at intervals longer than 1 hr ( Duncan 1949 ). Duncan’s experiments ushered in decades of work in many laboratories to define the time course of memory consolidation by studying ECS-induced retrograde amnesia. The data from these experiments, however, did not converge on a single time course that might have helped to identify the mechanisms underlying memory consolidation. Instead, the time course of memory consolidation appeared to vary widely depending on task parameters (for reviews, see Chorover 1976 ; McGaugh and Gold 1976 ).

Although the concepts of perseveration and memory consolidation remained central to the study of learning and memory (for reviews, see Glickman 1961 ; McGaugh and Herz 1972 ; Weingartner and Parker 1984 ), they would eventually be replaced by interference theory as an explanation for retroactive inhibition. Interference theory proposed that memories acquired close together in time compete for representational space, thereby interfering with each other. This theory readily accounted for the original observation of Müller and Pilzecker of a time-dependent disruption of original learning by interpolated material, and could also account for later findings, such as the fact that the degree of disruption increases with greater similarity between interpolated and original material (for reviews, see McGeoch and Irion 1952 ; Keppel 1984 ). 4 Thus, the perseveration theory of Müller and Pilzecker of memory consolidation fell out of favor within experimental psychology; however, their concepts eventually found considerable utility in biologically oriented studies of memory.

In 1949, in the light of emerging physiological data, Donald Hebb (1904–1985) advanced the dual-trace theory of memory formation. This theory revived the idea of perseveration by postulating a short-term memory in the form of reverberatory activity within local neural circuits. Reverberation was proposed to induce structural changes at synapses in the reverberating network and thus permit the memory to be stored more permanently ( Hebb 1949 ). Hebb’s ideas marked a shift in the approach to memory consolidation from manipulating memory in intact animals to studying the biological events that underlie the phenomenon of consolidation. For example, the postulate of structural change suggested a role for protein synthesis in the fixing of memory, which was confirmed by experiment ( Flexner et al. 1963 ; Agranoff and Klinger 1964 ; Barondes and Cohen 1965 ; for review, see Davis and Squire 1984 ). Today, it is thought that the phenomenon of memory consolidation in the minutes and hours after learning depends, in part, on a cascade of molecular events that lead to changes in the properties of neurons (e.g., Bailey and Chen 1983 ; Goelet et al. 1986 ; Alberini et al. 1994 ; O’Leary et al. 1995 ; Tully et al. 1995 ; Dudai 1996 ). These events include activation by second messenger cascades of transcriptional regulators, and multiple waves of mRNA and protein synthesis. Some of the proteins produce functional changes in neurons and synapses, whereas others lead to structural changes. In this sense, the ideas of Müller and Pilzecker can be traced from their origin to contemporary studies of the neuronal events that occur during a brief time period, shortly after learning.

Yet the term consolidation is also used today in the context of observations that memory can remain vulnerable to some manipulations for weeks, months, and even years after learning. In 1957, Scoville and Milner described severe anterograde and temporally limited retrograde amnesia following bilateral removal of medial temporal lobe structures. This finding led ultimately to the identification of the hippocampus and adjacent anatomically related cortical structures of the medial temporal lobe as components of a memory system that is essential for the formation of long-term memory ( Squire and Zola-Morgan 1991 ). Disrupting the function of this system causes retrograde amnesia, which is most severe for recent events and gradually less severe for remote events. Graded retrograde amnesia can extend across several years in humans ( Russel and Nathan 1946 ; Squire et al. 1975 ) and across weeks in mice ( Squire and Spanis 1984 ; for review, see Milner et al. 1998 ). Together, these findings suggest that medial temporal lobe structures contribute to the prolonged and gradual consolidation of memory over the course of weeks or even years. Specifically, the hippocampus has been proposed to direct a gradual process of reorganization and stabilization of representations in the neocortex (for reviews, see Squire and Alvarez 1995 ; Knowlton and Fanselow 1998 ). Although this process is likely to involve changes at synapses, it depends fundamentally on the successful interaction between the hippocampus and the neocortex and is distinct from the process by which synaptic efficacy is altered during the early phases of memory formation.

Müller and Pilzecker’s perseveration theory of memory consolidation was the starting point for discoveries of molecular and cellular events and brain systems important for memory formation. The neuronal events and processes that occur at the level of brain systems may unfold across different time scales, but all contribute to the dynamic and selective process of fixing memory over time. A challenge remaining for the next century is to understand, in detail, all the processes that underlie the phenomenon of memory consolidation—molecular and cellular events at synapses, the operations of brain systems, and the interactions among them.

Acknowledgments

We thank E.R. Kandel for his comments on earlier drafts of this manuscript. This work was supported by National Institutes of Health (NIH) grants NS19895 (J.H.B.), MH58321 (J.H.B.), NIH grant 24600 (L.R.S.), and the Medical Research Service of the Department of Veterans Affairs (L.R.S.).

↵ 1 Corresponding author.

↵ 2 The Science Citation Index lists 46 citations since 1955.

↵ 5 For biographical sketches and bibliographies, see Boring (1950) .

↵ 3 Earlier discussions of Müller and Pilzecker can also be found in McDougall (1901) ; Glickman (1961) ; and McGaugh and Herz (1972) .

↵ 4 Müller and Pilzecker themselves proposed an interference theory based on several experiments in which a cue syllable was trained with two different associates. These experiments showed that two associations with the same cue sylable were less well remembered than a single association. Müller and Pilzecker interpreted these findings as evidence for a competitive interference between the alternative syllables during acquisition and/or retrieval (see ).

Cold Spring Harbor Laboratory Press
Agranoff B.W. ,
Klinger P.D.
Alberini C.M. ,
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Kandel E.R.
Bailey C.H. ,
Barondes S.H. ,
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Burnham W.H.
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Squire L.R.
Duncan C.P.
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Flexner L.B. ,
Glickman S.E.
Goelet P. ,
Castellucci V.F. ,
Schacher S. ,
Weingartner H. ,
Parker E.S.
Knowlton B.J. ,
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McDougall W.
McGaugh J.L. ,
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Milner B. ,
Squire L.R. ,
Müller G.E. ,
Pilzecker A.
O’Leary F.A. ,
Byrne J.H. ,
Cleary L.J.
Russel W.R. ,
Nathan P.W.
Scoville W.B. ,
Spanis C.W.
Zola-Morgan S.
Slater P.C. ,
Boynton S.C. ,
Del Vecchio M.

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PERSEVERATION-CONSOLIDATION HYPOTHESIS

the hypothesis postulating that data goes through two phases in memory cultivation. During the first phase, the memory is retained by perseveration of neural activity and is simply disturbed. During the second phase, the memory comes to be fixed, or integrated, and is no longer simply disturbed. Commonly referred to as consolidation hypothesis- or consolidation-perseveration hypothesis.

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Review Article
Published: March 2009

A single standard for memory: the case for reconsolidation

Karim Nader 1 &
Oliver Hardt 1

Nature Reviews Neuroscience volume 10 , pages 224–234 ( 2009 ) Cite this article

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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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Rapid neural reorganization during retrieval practice predicts subsequent long-term retention and false memory

Engram neurons: Encoding, consolidation, retrieval, and forgetting of memory

Developmental differences in memory reactivation relate to encoding and inference in the human brain

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Acknowledgements

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.

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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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Memory consolidation is a dynamic process occurring over the lifetime of a memory, yet the underlying mechanisms are not well understood. The hippocampus is considered to be a critical structure for the acquisition, initial storage, and retrieval of a memory, but there is considerable debate over the continuing role of the hippocampus in representing a memory as it ages. Studies in rodents and humans both point towards a reorganization of hippocampus-dependent memory traces in the cortex over time, but when and how long it takes these large-scale network changes to occur is uncertain. In this chapter, we address how a memory that is initially dependent on the hippocampus becomes represented in the cortex, independently of the hippocampus. We also discuss how the quality of the memory changes (transforms) as the trace reorganizes over time, with a focus on hippocampal-cortical interactions as described by Trace Transformation Theory (TTT), and consider the degree to which evidence related to the mechanistic basis of memory consolidation in rodents applies to complex human memory. We conclude that theories like TTT provide a new approach to thinking about consolidation as an ongoing and interactive process involving the hippocampus, mPFC, and other brain regions.

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Time-dependent memory transformation along the hippocampal anterior–posterior axis

Retrieval of retrained and reconsolidated memories are associated with a distinct neural network

For this review, we will focus primarily on the type of memory that depends on the hippocampus for initial acquisition, including episodic memory in humans and episodic-like contextual and spatial memory in rodents.

Abbreviations

Anterior cingulate cortex

Cyclic-AMP response element binding protein

Immediate early gene

Late phase long-term potentiation

Medial prefrontal cortex

Medial temporal lobe

Multiple Trace Theory

Prefrontal cortex

Plasticity-related protein

Standard Consolidation Theory

Temporally-graded retrograde amnesia

Trace Transformation Theory

Functional magnetic resonance imaging

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Acknowledgements

The preparation of this chapter was supported by a grant to MM and GW from the Canadian Institutes for Health Research (CIHR—grant # MGP 6694). Research by the authors reported in this paper was supported by CIHR grant MGP 6694 and by grants from the Natural Sciences and Engineering Research Council to GW (# A8181) and MM (# A8347). MJS was supported by a CIHR post-doctoral fellowship.

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Sekeres, M.J., Moscovitch, M., Winocur, G. (2017). Mechanisms of Memory Consolidation and Transformation. In: Axmacher, N., Rasch, B. (eds) Cognitive Neuroscience of Memory Consolidation. Studies in Neuroscience, Psychology and Behavioral Economics. Springer, Cham. https://doi.org/10.1007/978-3-319-45066-7_2

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Memory Consolidation: Definition And Examples In Psychology

In memory consolidation psychology, memory and memory consolidation rely on a healthy body and brain. Many areas may affect your mind's ability to retain information, including age, substance use, medications, diseases, and mental health. Learning about these areas can be beneficial when trying to improve your memory consolidation ability.

Memory consolidation: Reinforcing memory traces

The memory consolidation process involves the storage of information in long-term memory. This occurs when memory traces are reinforced, stabilized, and saved so that we can later recall them.

What is a memory trace?

Also called an engram, a memory trace is a change in the nervous system that is thought to encode a memory. These memory traces assist us in reconstructing memories. After the memory trace is created, consolidation strengthens it through changes in neural pathways. The exact alterations that occur to create a memory trace are unknown; but research suggests that they are formed in the cerebellum and hippocampus .

How consolidation occurs

To understand the concept of memory consolidation, it may be helpful to think of memory as a muscle. Exercising your memory with repetition may help you retain memories over time and feel confident in recalling information. For example, perhaps you spent hours and hours in school studying and using the Pythagorean theorem. Doing so may have allowed you to exercise your brain to store the formula in your long-term memory. This process is called memory consolidation .

On the opposite end, placing your keys on the kitchen table when you get home and forgetting about them can be an example of a lack of memory consolidation. In this case, placing the keys down is an automatic gesture, so you may forget that you've done it. However, if you always place your keys on the same hook, your memory consolidation may allow you to know where they are when you leave the next day.

What are memories?

Memory is defined as the process of receiving information, storing details, and recalling that information later, all within the mind. Memory involves many portions of the brain, but the hippocampus, found within the brain's temporal lobes, is primarily responsible for emotions and memory .

This pattern of reactivation is a memory. Rather than memory being an organized system with separate compartments in the brain, it is an ever-changing system of neural patterns and pathways in which information travels across many brain regions.

In memory consolidation, recalling the same piece of information repeatedly trains the neurons to act together efficiently and rapidly. As this repetition continues, the neurons learn to fire together in the original pattern; thus, the information is more readily available in memory.

Theories of forgetting

For decades, experts in human memory have sought to explain the processes by which we experience memory failures. Theories of forgetting can help us understand how deficiencies in memory retrieval occur. While several other frameworks exist (e.g., repressed memories), the following are five of the most prominent theories of forgetting, separated by whether they impact short-term or long-term memory.

Forgetting information in short-term memory

Trace decay theory of forgetting .

An early theory of forgetting, the trace decay theory, posits that failing to retrieve a memory trace can cause it to deteriorate. According to the trace decay theory, all memories fade over time. When old memories decay, their retrieval becomes more difficult.

Displacement theory of forgetting

The displacement theory of forgetting states that the storage of new memories in short-term memory causes older information to be removed. This displacement occurs because of limited space in short-term memory.

Forgetting information in long-term memory

Retrieval failure theory of forgetting .

According to the retrieval failure theory, forgetting occurs when information in long-term memory is unable to be recalled. Proponents of this theory state that our memories are associated with certain memory cues, or retrieval cues. A retrieval cue may be a related image, word, sound, or other stimulus. When these retrieval cues are unavailable, we are not able to retrieve the information, and we experience a form of memory failure known as cue-dependent forgetting.

Interference theory of forgetting

The interference theory of forgetting is based on the idea that memories can be lost due to the formation or existence of other memories. These recent and remote memories can impact memory performance through two processes—proactive and retroactive interference. Proactive interference occurs when existing memories affect our ability to create new memories. Retroactive interference occurs when the formation of new memories interferes with our retrieval of existing memories.

Consolidation theory of forgetting

Focused on disturbances during the process of reinforcing memory traces, the consolidation theory of forgetting is associated with the physiological, instead of psychological, functioning of the memory system. According to the consolidation theory, interference with the consolidation process prevents memory traces from stabilizing, making retrieval more difficult. There are several ways consolidation can be disrupted, including medications, brain abnormalities, and lack of sleep. Consolidation theory has been backed by functional magnetic resonance imaging studies.

Causes of memory challenges

Before understanding memory consolidation, it may benefit you to understand the causes of memory challenges and memory loss that may cause difficulty with cognitive ability.

Age-related memory loss

As humans age, it can be natural for memory function to diminish gradually. Knowing that memories are constantly changing neural patterns, it can be easy to understand why no memories are permanent, including long-term and stored memories. Memory consolidation psychology shows many possible reasons that memory can decrease as people age. However, the two most common causes include reduced blood flow to the brain and deterioration of the hippocampus.

Other cases of memory decline can occur on a much more rapid and severe scale from certain diseases such as Alzheimer's. Alzheimer's disease is a form of dementia that progresses and irreversibly reduces an individual's mental functioning, including memory. Alzheimer's disease often leads to needing full-time care in the later stages of the progression. Dementia is a general term describing symptoms that significantly alter mental functioning.

Mental illness

Memory can be a vital part of personality and daily functioning. A few mental illnesses that impact cognitive ability may also lead to poor memory, including depression and anxiety. Those experiencing depression often report feeling as if their mind is foggy or clouded. When the brain is preoccupied with rumination and feelings of worry and anxiety, it can impair one's ability to form memories and learn new information.

Schizophrenia is another mental illness commonly associated with decreased memory function. One meta-analysis documented significant memory impairment in schizophrenia . According to the study, "the impairment was stable, wide-ranging, and not substantially affected by potential moderating factors such as the severity of psychopathology and duration of illness."

Substance use

Substance use may also cause significant interferences with memory consolidation and recall. Alcohol is one substance known for its potential memory interference, as it can lead to partial memory loss or complete blackouts if consumed in significant amounts.

Research is still being conducted on the ways that alcohol interferes with memory, but it is believed to be, in part, due to the disruptions that alcohol creates in the hippocampus. It is also shown that alcohol use interferes with neurons and their ability to respond to signals from other cells consistently. Benzodiazepines, often prescribed for acute anxiety, also have similar impacts on memory consolidation. This effect is often amplified in those who misuse benzodiazepines.

How to improve memory consolidation

According to memory consolidation psychology, the brain thrives on stimulation. Therefore, it is often said that learning new skills effectively cultivates brain health. For example, learning to play a musical instrument or speak a new language can exercise your brain and activate multiple areas.

Physical exercise is another proven way to boost mental functioning. The University of British Columbia conducted a study showing that regular aerobic exercise seemingly increased hippocampus size in older women with possible cognitive impairment. In addition, chronic inflammation can be linked to memory loss and cognitive decline later in life, and regular physical activity is linked to reducing inflammation in the body.

The quality of sleep you get is also associated with brain functioning and memory. Getting enough sleep can allow you to better process, consolidate, and store new information as memories in the brain. Memory loss or difficulty remembering information is also often associated with sleep deprivation, sleep apnea, and other sleep-related disorders such as narcolepsy.

Counseling options

Experiencing difficulties with processing and retaining memory can be unsettling and, in some cases, frightening. If you are struggling with memory loss or other concerns about cognitive function, speak to a doctor immediately. A neurologist can help you isolate the potential causes of your symptoms and begin treatment if necessary.

If you discover that your memory issues could be related to a mental health condition like depression or anxiety, contacting a therapist may also be beneficial. A psychologist can use methods like cognitive-behavioral therapy (CBT) to isolate the root cause of your challenges and provide you with tools to cultivate a healthier state of mind and a more significant capacity for memory retention.

The rise of online therapy in treating anxiety, depression, and trauma-related disorders has removed many common barriers to therapy that keep people from getting help. For instance, online therapy is often more convenient, flexible, and affordable than in-person therapy. Studies have backed up these claims, showcasing the cost-effectiveness of internet-based interventions.

Online platforms like BetterHelp match clients with mental health professionals with experience in various specialized care. You can speak with a counselor via phone, text, video chat, or online messaging to get started as you move toward better mental health.

What Is Insight? Definition, Psychology, And Practical Examples Medically reviewed by Kimberly L Brownridge , LPC, NCC, BCPC
Understanding Prejudice: Origins, Mental Health Impact, And Ways To Combat Bias & Discrimination Medically reviewed by Nikki Ciletti , M.Ed, LPC
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Bermúdez-Rattoni F, editor. Neural Plasticity and Memory: From Genes to Brain Imaging. Boca Raton (FL): CRC Press/Taylor & Francis; 2007.

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Chapter 11 memory reconsolidation or updating consolidation.

Carlos J. Rodriguez-Ortiz and Federico Bermúdez-Rattoni .

11.1. INTRODUCTION

For a long time, consolidation was seen as a process achieved only on newly acquired memories aimed to store them for the long term. However, pioneer and recent studies have demonstrated that after retrieval, long-term memories may once more undergo a consolidation-like process referred to as reconsolidation. Mainly, reconsolidation is sustained by the now widely reported observation that after a memory trace is activated by means of retrieval and is susceptible to disruption by the same treatments that disrupt memory during consolidation. However, the functional purpose of this process is still a matter of debate.

Recent evidence indicates that reconsolidation is indeed a process by which updated information is integrated through the synthesis of proteins to a memory trace. Hence, the so-called reconsolidation seems more like an updating consolidation intended to modify retrieved memory by a process that integrates updated experience into long-term memory. Through this process, previously consolidated memory is partially destabilized. By the infusion of disrupting agents, it appears as if the process is intended to consolidate memory again. In this chapter, we discuss this issue and propose that updating consolidation is a more descriptive term for this process.

11.2. CONSOLIDATION HYPOTHESIS

The classification of memories according to their duration was initiated by Hermann Ebbinghauss in his work titled “Uber das Gadachtnis” (About Memory) and formalized later by William James. From these works it appears that memory has, on the basis of its time course, at least two forms, namely short- and long-term memories. Although no fixed time span segregates these two memory forms, it is clear that information stored in long-term memory (LTM) undergoes a consolidation process that strengthens it over time into a stable memory trace.

This process does not take place for short-term memory (STM), which decays much sooner. The term consolidation is acknowledged to Müller and Pilzecker on their study reported in 1900. In one set of experiments, they trained subjects to memorize a list of paired syllables. On the test day, cue syllables (each one was a single syllable of a pair) were presented and the number of complementary recalled syllables was used as a measure of memory retention. A reduction in the number of retrieved syllables from the first list was observed if a second (distracting) list of syllables was presented shortly after training. Furthermore, the longer the interval between the two lists, the less the performance was affected. The researchers concluded that the second list interfered in a time-dependent manner on a physiological process that accounts for the strengthening of memories. They named this process “consolidirung.” 1

These observations were mostly ignored until Duncan reported almost 50 years later that he proved that an electroconvulsive shock (ECS) applied after training disrupted memory. Moreover, he showed that memory disruption correlated with the interval between training and ECS application. Since ECS was longer spaced in time from training, memory impairment was reduced. Since then, several other researchers have shown that interfering treatments — from ECS to intracerebral microinjections of protein synthesis inhibitors — applied after acquisition prevent LTM storage. Consistently, LTM is not affected if the intrusive treatment is applied outside the vulnerability window. This, along with the consolidation hypothesis, led to the idea that memory undergoes this time-dependent stabilization process only once. Reliability among a huge amount of related studies sustained the prominent place that this idea occupies in the current model of consolidation. 2 , 3

An important transition in memory research took place after Hebb’s dual-trace proposal suggesting that memory is at first in a labile state maintained by a reverberating neural ensemble. LTM arises from cellular changes in this ensemble allowing memory stabilization. 4 Although it is still matter of intense debate whether STM and LTM are serial or parallel processes, dual-trace theory stressed the weight that cellular entities have in memory processing, turning research to the cellular events underlying memory. At the cellular level, STM undergoes activation of transduction * cascades (mainly kinase pathways) after neuronal stimulation. It is proposed that STM remains as long as these cascades are active but for LTM, transduction signals are carried to the nucleus where transcription * is achieved. Afterward, RNA translation † will ultimately lead to protein synthesis. These proteins account for cellular plastic changes that are considered the cellular correlations of stable LTM traces, i.e., they are considered the cellular counterparts of consolidation. Hence, memory consolidation requires protein synthesis. It has been extensively reported that protein synthesis inhibition disrupts LTM without affecting STM. 3 , 7–9

11.3. RECONSOLIDATION ERA

As noted earlier, consolidation was seen as a process achieved only on newly acquired memories with the intent of long-term storage. However, pioneer studies indicated that consolidated memories may undergo a consolidation-like process more than once under certain conditions. In 1968, Misanin et al. 10 habituated rats to lick from a drinking bottle in a conditioning chamber, after which they were trained in a fear conditioning task in which a tone (conditioned stimulus, CS) was paired to a footshock (unconditioned stimulus, US). As a result, a conditioned response was obtained and used as a measure of memory, in this case, a reduced licking rate from the water bottle after the tone onset. They reported that an ECS applied immediately after conditioning disrupted memory consolidation ( Figure 11.1b , Group 2). The interesting point arose from Group 3. Those animals were trained but without delivery of an ECS. A day later, the consolidated fear memory was reactivated by presenting the tone again. Immediately after this memory reactivation, an ECS was applied with the surprising result that memory was impaired when tested 24 hours later ( Figure 11.1b , Group 3). Notably, ECS was unable to disrupt memory if the tone cue was not presented ( Figure 11.1b , Group 4) and the phenomenon was referred as cue-dependent amnesia. 10

FIGURE 11.1

Data from first report on retrograde amnesia induced after memory reactivation. (a) Schematic representation of protocol used by Misanin et al. (b) Group 1 shows fear conditioning behavior displayed under this protocol, measured as reduced licking from (more...)

Even though these results were at first not replicated, 11 they encouraged further (mainly unnoticed) work on the possibility that consolidated memories enter into an active stage upon retrieval. For example, Gordon showed that as occurs with newly acquired memories, retrieved memories are susceptible to disruption in a time-dependent manner. 12 Cue-dependent amnesia was further studied in the active–inactive memory model proposed by Lewis. 13 who claimed that memories become active under two conditions: when newly acquired and when reactivated by means of retrieval. Any other memory is in an inactive stable state. Recently, cue-dependent amnesia was taken up again and is now referred as reconsolidation.

Reconsolidation proposes that after a memory trace is activated by means of retrieval, it is susceptible to disruption by the same treatments that disrupt memory during consolidation. 14 , 15 In 1992, Bucherelli and Tassoni 16 reported that inactivation of the parabrachial nuclei by infusions of tetrodotoxin disrupted previously consolidated memories when reactivated. Similarly, Susan Sara’s group reported that infusions of either NMDA or β-adrenergic antagonists (which disrupted LTM when applied after training) disrupted a clearly established memory trace upon retrieval. 17–19 Since then, memory reconsolidation has actively been studied.

The most acknowledged study is the one carried out by Nader and coworkers in 2000. 20 This work brought general attention to the reconsolidation phenomenon because of the clean data reported and because of the use of a translational inhibitor that interfered with protein synthesis, considered to be the main cellular substrate for memory consolidation. The experiments were performed in the widely studied fear conditioning task and showed that the same treatment applied under circumstances that disrupt consolidation also impairs memory after retrieval. Similar to the report by Misanin and coworkers, Nader et al. conditioned rats in a tone-foot-shock association but memory was assessed by the percentage of the time that rats were immobile (except for movements required for breathing) to the total time the tone was presented (freezing). The day after conditioning, the protein synthesis inhibitor anisomycin was injected in the amygdala after the tone presentation.

When the subjects were tested 24 hours later, they performed poorly compared to the rats that were not anisomycin-injected ( Figure 11.2b ). The same treatment was unable to disrupt memory if a retrieval session was not performed ( Figure 11.2b , Group 3). The researchers also showed that the effects of anisomycin were time-dependent. When injected 6 hours after memory reactivation, it is unable to disrupt memory. In the years following the Nader study, a wide variety of reports have shown that reconsolidation is indeed a general process achieved in different species and different kinds of memories. 21–30

FIGURE 11.2

Intraamygdalar infusion of a protein-synthesis blocker disrupts consolidated fear memory. (a) Schematic representation of protocol used by Nader et al. (b) Group 1 shows fear conditioning behavior displayed under this protocol, measured as high percentage (more...)

11.4. ON RESTRAINTS OF RECONSOLIDATION HYPOTHESIS

Despite the huge body of experiments supporting reconsolidation, some did not uncover consolidated memory susceptibility to disruption after retrieval. 31–34 However, some recent reports have helped explain to an extent why a reconsolidation process is not revealed under certain protocols. 26 , 35 , 36 To address this issue, we must first look to what is called extinction and again take up the conditioning protocol on which a great number of memory tasks rely. On conditioning, a CS, like a tone, is associated to an US, like a foot shock. As a result, the CS elicits a response that is used as a measure of memory, like freezing.

However, CS presentation in the absence of US eventually leads to a response decrement; in our example, animals stopped freezing. This is extinction. On extinction, the CS is now associated to no-US. Like any other learning, extinction undergoes consolidation. To assess reconsolidation, the CS is commonly presented as a retrieval cue that may lead to extinction. During testing, treatments applied on retrieval may reflect effects over the CS-US association in which case disruption of the conditioned response is observed (reconsolidation is uncovered).

On the other hand, treatments may impair consolidation of extinction, in which case the CS-US association seems unaltered. On this latter scenario, results may be interpreted as lack of a reconsolidation process. Hence, studies like Vianna et al. 32 and Berman and Dudai 31 reported that protein synthesis inhibition disrupted extinction, leaving CS-US association unimpaired or even strengthened, and pointing at the impression that reconsolidation does not occur under these protocols.

Pedreira and Maldonado 35 offered evidence to move forward using a contextual memory task in crabs. When crabs are placed in a particular context and an object is passed overhead, they escape from the moving object, but when this stimulus is repeated several times, the crabs freeze upon presentation of the passing object. However, when the context is changed, freezing of the crabs does not take place. Thus, the context is associated to the passing object and freezing is used as a measure of memory. To induce extinction, the animals were exposed to the context in the absence of the passing object. Pedreira and Maldonado placed conditioned crabs in the training context for either 5 or 60 min as a retrieval session. During the session, they systemically applied the protein synthesis inhibitor cycloheximide and tested 24 hours later. Crabs exposed for 5 min did not undergo a clear extinction and when tested, effects over reconsolidation were found. Conversely, crabs exposed for 60 min extinguished the conditioned response and when tested, extinction was impaired.

These findings have been replicated by many others. 26 , 36 Eisenberg et al. 26 trained rats in a taste aversion task. Task acquisition was achieved by pairing a taste with an intraperitoneal injection of a visceral malaise-inducing agent (LiCl). Taste–malaise association produced a long-term aversive memory observed by a reduced intake of that taste in a second presentation compared to its consumption on acquisition. However, on the third presentation, intake was increased, showing that the aversive memory was extinguished. Protein synthesis inhibition disrupted extinction when applied on the second taste presentation leaving CS-US pairing unaltered, i.e., a failing to detect a reconsolidation process.

However, when rats were subjected to the taste–malaise association for two consecutive sessions, extinction was not observed on the subsequent presentations. Under these conditions, protein synthesis inhibition on the presentation following the association sessions showed aversion impairment when the animals were tested, i.e., reconsolidation was revealed. In the same study, medaka fishes were trained in a fear conditioning task. Consistent with the results obtained from rats, protein synthesis inhibition impairs consolidation on the session that led to extinction affected and, in the absence of extinction, protein synthesis inhibition impaired CS-US reconsolidation. Thus, when consolidation of extinction memory was initiated on the retrieval session, reconsolidation of the CS-US association was not observed.

Other authors have found that pharmacological treatments disrupted LTM of recently consolidated but not older consolidated memories. 37 , 38 That is, when the retrieval session takes place on the days following acquisition, memory is susceptible to consolidation blockers. However, as the retrieval session is spaced in time from training, memory becomes less sensitive to these blockers. These results point to the idea that reconsolidation is a process achieved only by recently consolidated memories upon retrieval. However, Suzuki and co-workers 36 reported that stronger and older memories are susceptible to disruption upon retrieval too. They showed that stronger and older memories need of a longer retrieval trial to be disrupted by the blockade of protein synthesis than weaker and younger memories. Consistent with the reports of Pedreira and Maldonado 35 and Eisenberg et al., 26 these effects were found as long as the retrieval trial did not lead to extinction. Therefore, it seems that the strength of the reminder is related to memory susceptibility to disruption after retrieval.

11.5. CONSOLIDATION AND RECONSOLIDATION: THE SAME PROCESS?

Probably the most important question regarding the reconsolidation process is: why and under what circumstances is reconsolidation attained? At first glance, it seems counterintuitive to carry out an already achieved process again, i.e., to consolidate once more an already consolidated memory, as is implied by the reconsolidation term. It has been reported that some of the molecular mechanisms involved in consolidation are also required for reconsolidation of the same memory trace and in the same brain region. 20 , 23 , 24 , 26 , 39–43 For example, particular transcription factors have been proven necessary for both consolidation and reconsolidation processes in different memory tasks. Kida and colleagues 40 showed CREB involvement in contextual fear conditioning * memory in mice. Also in mice, Bozon and co-workers 41 reported a zif268 requirement in object recognition memory † and finally, Merlo et al. 42 showed NF-B participation in contextual memory using the crab model described above. In rats, Duvarci, Nader, and LeDoux 43 showed that the extracellular signal-regulated kinase (ERK) pathway must be activated in the amygdala for both consolidation and reconsolidation of fear conditioning. Furthermore Sangha et al. 24 reported that for the Lymnaea stagnalis snail, consolidation and reconsolidation occurred in the same cell. These data indicate that reconsolidation may be a remaking of the consolidation process. 15

However, several other studies suggest that consolidation and reconsolidation are different processes. Taubenfeld and colleagues 44 reported that the transcription factor C/EBPβ is needed for consolidation but not for consolidation of a context-dependent task in the dorsal hippocampus. Tronel and Sara 45 described differential activation of several brain regions after retrieval compared to consolidation of an odor-reward task learning analyzed by c/Fos immunohistochemistry. In the same regard, Kelly and co-workers 28 demonstrated an increase in phosphorylation of ERK kinases in the dentate gyrus and the entorhinal cortex after training in an object recognition task along with increased phosphorylation in the hippocampal CA1 region and the entorhinal cortex after memory retrieval. On taste memory, it was reported that muscarinic receptor activity in the gustatory cortex is required for safe memory consolidation but not for postretrieval consolidation. 46 Similarly, protein synthesis in the central amygdala is required for consolidation but not for reconsolidation of conditioned taste aversion. 47 Finally, Lee et al. 48 reported that the growth factor BDNF is required for consolidation but not for reconsolidation, and transcription factor zif268 is needed for reconsolidation but not consolidation in the same brain region and memory task. All this evidence discards the possibility that reconsolidation is a recapitulation of consolidation but does not solve the problem. The question remains: what is the physiological purpose of reconsolidation?

11.6. RECONSOLIDATION HYPOTHESIS RECONSIDERED: UPDATING CONSOLIDATION PROPOSAL

Early and recent reviews suggest that reconsolidation may be a state for incoming information to modify established memories but experimental support is almost completely absent. 13 , 14 , 49 , 50 However, our group recently reported that newly acquired and retrieved taste recognition memory is susceptible to disruption by the protein synthesis inhibitor anisomycin when applied in the insular cortex (IC), a proven site for taste memory consolidation. In that work, the attenuation of neophobia (AN) task was used. Animals showed graded increases in intake after repeated presentations of the same tastant until a plateau was reached ( Figure 11.3a ). 51 , 52

FIGURE 11.3

Attenuation of neophobia (AN) behavior and protein synthesis inhibition effect (a) Mean ± S.E.M. intake (in mL) of 0.3% saccharin solution on unoperated rats. Taste presentations were daily for 15 min. (b) and (c) Anisomycin infusion in insular (more...)

Importantly, anisomycin injections produced a partial disruption of previously consolidated memory and the observed impairment became less noticeable as a response plateau was reached ( Figure 11.3b and c ). On asymptotic performance, anisomycin affects no longer consolidated memory ( Figure 11.3d ). These results led to the proposal that a protein-synthesis-dependent process is achieved as long as updated experience capable of affecting behavior is acquired. This process is aimed to integrate updated relevant information to LTM. Consistently, part of the older consolidated memory is dependent on protein synthesis. Partial susceptibility to disruption of a previously consolidated memory trace may be the physiological substrate that allows incoming material to integrate to memory.

Furthermore, when there is no more relevant information to be learned, i.e., after asymptotic task performance is reached, memory is no longer vulnerable to protein synthesis inhibition. Moreover, when the AN plateau has been reached and information of a different quality is provided, like aversive information, the protein-synthesis-dependent process is achieved once more ( Figure 11.3e ). 53

These results were partially replicated in a widely studied hippocampus-dependent memory task, the Morris water maze (WM). In this task, animals escape from cool water by finding a hidden platform underwater. To do so, animals learn spatial cues around the room to locate the platform. 54 Rats were trained for either 3 or 5 consecutive days in the WM task. Seven days later on the memory reactivation session, rats swam for 60 sec without the platform and memory was assessed by counting the number of crossings to the platform location during training.

Clearly, the animals trained for 5 days performed much better than those trained only for 3 days. Thus, 3-day trained rats were designated middle-trained and 5-day trained rats were referred to as well-trained. When tested 7 days after the reactivation session, middle-trained subjects infused with a consolidation blocker in the dorsal hippocampus on reactivation performed poorly compared to the corresponding vehicle group. However, the same treatment did not affect consolidated memory in well-trained animals, presumably because no further updating was attained. 55 Similarly, Morris et al. 56 reported that asymptotic WM task performance was not affected by protein synthesis inhibition in the dorsal hippocampus.

Conversely, task performance was disrupted by the same treatment when updating information was continuously acquired. They trained rats for 6 days in the WM task with the platform in a constant position. On day 7, retrieval was accounted by a single trial and anisomycin was immediately injected locally. Under these conditions memory was unimpaired. Interestingly, when the platform location was changed daily during training, anisomycin injection after retrieval on day 7 disrupted previously consolidated memory. The authors concluded that acquisition of new information is required to observe consolidated memory susceptibility to protein synthesis inhibition.

Thus, the so-called reconsolidation seems more like an updating consolidation intended to modify retrieved memory by a process that integrates updated experience into long-term memory. Previously consolidated memory is partially destabilized and by the infusion of disrupting agents it appears as if the process is intended to consolidate memory again. Two important features must be stressed about the updating consolidation process: it is time- and protein-synthesis-dependent. These features again bring attention to the cellular changes that account for LTM, i.e., the stabilization of neural ensembles. 4

Updating consolidation may be the process by means of which neural ensembles are modified and stabilized into updated memory traces. This proposal is based on the analysis of behavior, and even though it is clear that behavior is not merely a reflection of memory; we think it is possible to outline some of the changes that the updating consolidation process may produce in the memory traces based on the behavioral observations depicted above (for more on the behavior–memory dichotomy see Chapter 1 ). In a simple scenario, two types of information can modify behavior.

Reinforcement of previous learning

As with a learning curve, previous learning is strengthened on each trial because information of the same quality is acquired. Keeping in mind that a neuronal ensemble underlies a particular memory, reinforcing information may modify the existing consolidated trace by two means: by making the synaptic weights of the already existing ensemble stronger or by addition of cellular entities to the previously consolidated ensemble. In both cases, modifications of the synaptic weights involved in the ensemble are required.

Using artificial neural network simulation, it has been proposed that in order to preserve old memories while learning sequential new patterns, an active maintenance process is required. Otherwise, old memory is lost with incoming information. In this model, new learning is incorporated to old patterns by partially rehearsing the old ones. Importantly, modifications in synaptic weights are needed if the ensemble is to retain previously stored material while learning new information. 57

Updating consolidation is the proposed mechanism that permits modifications of the ensemble. By protein synthesis inhibition, updating consolidation is unveiled in the limited disruption of previously acquired information that is less noticeable as plateau performance is reached. Consistently, lack of memory disruption by protein synthesis inhibitors correlates with the asymptotical level in task performance. In this regard, positive modulation of a retrieved memory was reported in crabs. 58 The study showed that through retrieval, a weak memory is strengthened by an endogenous brain mechanism mediated by angiotensin II. Although, positive modulation of retrieved memories has been reported, 14 , 59 this study was done to shed light upon the functional value of reconsolidation. In accordance with the updating consolidation proposal, the researchers concluded that reconsolidation is a state for modifying memory strength.

A last piece of evidence comes from memory studies in chicks. Summers et al. 60 reported that a weak memory is strengthened by means of retrieval. They suggested that memory retrieval initiates a mechanism that allows incorporation of information acquired in the retrieval session to LTM. However, memory retrieval was found to modify memory as long as consolidation was not accomplished. Thus, this mechanism in chicks seems limited to the time before memory is stored. 60 , 61 This is not the case in rats, where memory can be modified after consolidation is attained and even more, as noted above, limited disruption of previously consolidated memory is observed.

Shift of previous learning

Divergent information is integrated to previously consolidated memory. For example, taste aversion can be learned from a taste already tagged as a safe stimulus. 53 , 62 Under these conditions, taste aversion requires a protein synthesis-dependent process to be stored in the long term. One possibility for this integration to occur is that the ensemble suffers greater modifications than when strengthening information is acquired. On the other hand, a different but overlapping trace would be created for this divergent information, in which case modifications in the synaptic weights involved in the first ensemble would take place as well. Overlapping between the ensembles is supposed because they represent divergent associations between overlapping stimuli. In our taste memory example, this overlapping is uncovered on the aversion level that animals show to a taste previously tagged as safe ( Figure 11.3e ). Less aversion is observed when compared to the aversion shown to the same taste when novel. Reinforcement of aversive learning is required to reach similar aversion levels when the taste was previously learned as safe.

Another example has been reported in the Manduca sexta moth. Daly and colleagues 63 found progressive neural recruitment and changes on network activity over the course of olfactory conditioning. Their results point to the idea that olfactory memory traces are modified upon experience. Hence, memories are not separate entities; rather they overlap to some extent. Overlapping of the traces is determined by the similarities of the involved information. This idea is in line with previous theories regarding incorporation of recent experiences into long-term knowledge background. 64–66

Extinction is another possibility in which a memory trace can be updated by divergent information. Ample evidence indicates that extinction is not forgetting nor erasing of conditioning learning, but a related learning that elicits a behavioral shift upon CS presentation. 67 This evidence is congruent with the proposed model of updating consolidation. Updating does not imply erasing of previous learning but incorporation of a related learning that takes over behavior. 53

Eisenberg and Dudai 38 consistently reported that disrupted memory upon retrieval is recovered by presentation of an unpaired reinforcer. Similarly, contextual conditioning memory disrupted after retrieval was shown to recover spontaneously after 21 days. 68 Power et al. 69 found contextual-conditioning memory recovery 6 days after acquisition and, moreover; using the same memory task, Prado-Alcalá et al. 70 reported that repeated retrieval sessions are sufficient to fully recover memory previously affected on retrieval by tetrodotoxin injections.

These results suggest that disruption of the reconsolidation process does not abolish consolidated memory; instead, the observed memory destabilization known as reconsolidation may be related to interference with the proposed updating process aimed at the integration of related learning. The result of this process will be stable overlapping traces. The relationships of these converging (trace reinforcement) or diverging (trace shift) overlapping traces will determine behavior.

Recently, it was reported that reconsolidation and integration of new information to memory are dissociable processes. Animals were conditioned using a light and a context as CSs, and footshocks as USs. On retrieval, a new context and the same light were presented without the US. As a consequence, an association was established between the first conditioning, i.e, the first CS-US association, and the new context. When tested, animals elicited the conditioned response (freezing) when placed in the second context, that is, a new CS.

The association between a CS and a previously acquired CS-US association is called second order conditioning. Inhibition of the transcription factor C/EBPβ in the hippocampus disrupted LTM of the second conditioning. Conversely, if retrieval is assessed presenting the same stimuli as in acquisition C/EBPβ is required in the amygdala for memory to remain. Thus, it was concluded that linking new of information occurs without destabilizing the retrieved memory. 71

Contrary to this, we found in two different memory tasks and regions that partial disruption of consolidated memory is observed by consolidation blockers upon memory updating. Moreover, protein synthesis is still required in the same region even though updated information is of different quality. It is important to note that the differences in molecular mechanisms found by Tronel et al. 71 indeed support the view that linking new information is not the same as reinforcement of previous learning (as reconsolidation is not a bona fide copy of consolidation), but do not support that reconsolidation is not intended to update memory.

The important issue is that reinforcement of previous learning is not synonymous with reconsolidation and that linking new information is different from a reconsolidation process. On their retrieval protocol, Tronel et al. used either the same (which they called reconsolidation) or different information (another context they called linking new information) compared to acquisition. Integration of information of one kind does not necessarily imply that integration of another kind requires the same mechanisms. All in all, we consider that evidence is accumulating for the hypothesis that reconsolidation is indeed an updating consolidation. In this time- and protein-synthesis-dependent process, retrieved memory seems to be modified by the integration of updated relevant experience.

ACKNOWLEDGMENTS

We thank Oreste Carbajal for technical assistance. Part of the work described in this chapter was supported by CONACYT-México 42657/A-1 and DGAPA.-UNAM IN-220706-3.

Process by which a cell converts an extracellular signal into a response. 5

Synthesis of RNA on DNA template. 6

Synthesis of protein on mRNA template. 6

In this protocol, a context (CS) like a particular chamber is associated with a footshock (US). As with fear conditioning, the response used as a measure of memory is freezing (in this case, a reaction to the chamber, not to a tone).

This kind of memory reflects the judgment of previous experience with particular stimuli. The tasks commonly rely on the natural tendency of rodents to explore new stimuli. In the first phase, animals are habituated to a novel stimulus like a light bulb. After a delay, the second phase involves presentation of a copy of the bulb along with some other stimulus like a glass jar. During this phase, the animals explore the jar over the bulb, indicating that the jar is a new stimulus and the bulb a familiar one, that is, the bulb is recognized as a familiar stimulus.

Cite this Page Rodriguez-Ortiz CJ, Bermúdez-Rattoni F. Memory Reconsolidation or Updating Consolidation? In: Bermúdez-Rattoni F, editor. Neural Plasticity and Memory: From Genes to Brain Imaging. Boca Raton (FL): CRC Press/Taylor & Francis; 2007. Chapter 11.

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INTRODUCTION
CONSOLIDATION HYPOTHESIS
RECONSOLIDATION ERA
ON RESTRAINTS OF RECONSOLIDATION HYPOTHESIS
CONSOLIDATION AND RECONSOLIDATION: THE SAME PROCESS?
RECONSOLIDATION HYPOTHESIS RECONSIDERED: UPDATING CONSOLIDATION PROPOSAL

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Consolidation

Consolidation refers to the process by which memories are strengthened and stabilized in the brain. It involves transferring information from short-term memory to long-term memory storage.

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Practice Questions ( 5 )

Which of the following experiments would best test the hypothesis that sleep deprivation disrupts the consolidation of long-term memories?
How does sleep affect consolidation of declarative memories?
Which of the following best exemplifies the process of consolidation in Neuropsychology?
What experiment would best examine the impact of sleep deprivation on the consolidation of episodic memories?
Which region would be targeted by an intervention aiming to aid consolidation from short-term to long-term memory for someone with anterograde amnesia?

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Encoding : The initial process of acquiring information and transforming it into a format that can be stored in memory.

Retrieval : The process of accessing and recalling stored information from memory.

Hippocampus : A brain structure involved in the formation and consolidation of new memories.

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COMMENTS

Memory consolidation
Memory consolidation is a category of processes that stabilize a memory trace after its initial acquisition. [1] A memory trace is a change in the nervous system caused by memorizing something. Consolidation is distinguished into two specific processes. The first, synaptic consolidation, which is thought to correspond to late-phase long-term ...
APA Dictionary of Psychology
the hypothesis that information passes through two stages in memory formation. During the first stage, the memory is held by perseveration (repetition) of neural activity and is easily disrupted. During the second stage, the memory becomes fixed, or consolidated, and is no longer easily disrupted. The perseveration-consolidation hypothesis ...
Consolidation and reconsolidation: Two lives of memories?
Consolidation as linking cortical representations . There are several variations of the hypothesis that the hippocampus rapidly stores critical information for linking cortical representations and that during multiple iterations of cortical-hippocampal interaction, connections within the cortex are strengthened and eventually support these associations in the absence of hippocampal function ...
What Is Memory Consolidation?
Memory consolidation relies on synapses in the brain. In something akin to an electrical system conducting a current,r the synapses pass signals from neuron to neuron with the help of neurotransmitters. The more frequently signals are passed, the stronger the synapses become. This process, called potentiation, is believed to play a major role ...
12 Two Distinct Stages of Memory Consolidation
The consolidation hypothesis received little attention in the twentieth century until the later 1940s, when studies showed that electrical currents applied to the head sufficient to produce overt convulsions (electroconvulsive shock; used successfully to treat psychiatric disorders such as major depression) produced a retrograde amnesia.
Memory Consolidation
Systems consolidation is typically, and accurately, described as the process by which memories, initially dependent on the hippocampus, are reorganized as time passes. By this process, the hippocampus gradually becomes less important for storage and retrieval, and a more permanent memory develops in distributed regions of the neocortex.
Memory Consolidation
Memory consolidation is a fundamental process of long-term memory formation, as, in fact, has been described to occur in a multitude of different types of memories, species, and memory systems. It refers to the stabilization process of a newly formed long-term memory. Initially, the memory is in a fragile state and can be disrupted by several ...
Memory--a century of consolidation
Abstract. The memory consolidation hypothesis proposed 100 years ago by Müller and Pilzecker continues to guide memory research. The hypothesis that new memories consolidate slowly over time has stimulated studies revealing the hormonal and neural influences regulating memory consolidation, as well as molecular and cellular mechanisms.
Memory Consolidation
The view of consolidation advanced by the pioneering experimental psychologists Müller and Pilzecker was not embraced by the field of experimental psychology in the latter half of the twentieth century. Ironically, during that same period of time, the notion that memories consolidate became the "standard story" in the field of neuroscience.
100 Years of Consolidation— Remembering Müller and Pilzecker
The origin of the concept of memory consolidation and the introduction of the term "consolidirung" (consolidation) to the modern science of memory are generally credited to Georg Elias Müller (1850-1934), professor at the University of Göttingen, Germany, and his student Alfons Pilzecker. Their seminal monograph "Experimentelle ...
Memory consolidation.
This chapter introduces the concept of multiple memory systems, which brain structures are engaged, and how they interact through the process of consolidation. Memory consolidation takes place both at the microscopic level, in the form of changes in synaptic strength, and at the whole-brain systems level, where it refers to a representational shift between different neural networks. We focus ...
Reconsolidation and the Dynamic Nature of Memory
Reconsolidation, as we discussed above, has been defined by applying the very standards that define consolidation. Therefore, certain nonspecific interpretations of the reconsolidation hypothesis pose the same challenges to the consolidation hypothesis, a consequence that is rarely acknowledged.
PERSEVERATION-CONSOLIDATION HYPOTHESIS
the hypothesis postulating that data goes through two phases in memory cultivation. During the first phase, the memory is retained by perseveration of neural activity and is simply disturbed. During the second phase, the memory comes to be fixed, or integrated, and is no longer simply disturbed.
A single standard for memory: the case for reconsolidation
As a consequence of the perceived inability of the consolidation hypothesis to account for reconsolidation, new memory models were developed that treated new and reactivated consolidated memories ...
Mechanisms of Memory Consolidation and Transformation
One proposed mechanism is the 'active consolidation in sleep' hypothesis. ... but it is clear from the dictionary definition of the term consolidation, 'to make firm', that it is a misnomer. Cellular consolidation, systems consolidation, and reconsolidation are all part of a dynamic, non-linear process. ... Department of Psychology and ...
Memory Consolidation: Definition And Examples In Psychology
Also called an engram, a memory trace is a change in the nervous system that is thought to encode a memory. These memory traces assist us in reconstructing memories. After the memory trace is created, consolidation strengthens it through changes in neural pathways. The exact alterations that occur to create a memory trace are unknown; but ...
Memory Consolidation
Memory consolidation in psychology is how the brain transforms short-term memories into long-term memories. The main characteristics of the memory consolidation process include the following:
Memory Consolidation
Memory consolidation is a fundamental process of long-term memory formation, as, in fact, has been described to occur in a multitude of different types of memories, species, and memory systems. It refers to the stabilization process of a newly formed long-term memory. Initially, the memory is in a fragile state and can be disrupted by several ...
Memory integration: An alternative to the consolidation/reconsolidation
The theoretical hypothesis is derived from the idea that newly formed memories are initially labile and sensitive to disruption, but over time undergo a time-dependent 'consolidation' process that converts them into a stable form largely resistant to disruption (Fig. 2).As a consequence, the consolidation hypothesis posited that, once memory was consolidated into storage, amnesia could not ...
Memory Reconsolidation or Updating Consolidation?
For a long time, consolidation was seen as a process achieved only on newly acquired memories aimed to store them for the long term. However, pioneer and recent studies have demonstrated that after retrieval, long-term memories may once more undergo a consolidation-like process referred to as reconsolidation. Mainly, reconsolidation is sustained by the now widely reported observation that ...
APA Dictionary of Psychology
A trusted reference in the field of psychology, offering more than 25,000 clear and authoritative entries. ... consolidation. Share button. Updated on 04/19/2018. ... See perseveration-consolidation hypothesis. Browse Dictionary.
Systems Consolidation
Learning and memory. In Fundamentals of Cognitive Neuroscience, 2013. 3.3 System consolidation: interaction between the medial temporal lobes and the neocortex. System consolidation can take much longer to complete and may range from days to years or decades. Patients with MTL lesions show a retrograde memory loss that is temporally graded, so recent memory loss (before the amnesia) is greater ...
Consolidation
AP Psychology; Consolidation; Consolidation. Definition. Consolidation refers to the process by which memories are strengthened and stabilized in the brain. It involves transferring information from short-term memory to long-term memory storage. ... Practice Questions (5) Which of the following experiments would best test the hypothesis that ...

What Is Memory Consolidation?

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Memory Consolidation: Definition And Examples In Psychology

Memory consolidation: Reinforcing memory traces

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How consolidation occurs

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Forgetting information in short-term memory

Displacement theory of forgetting

Forgetting information in long-term memory

Interference theory of forgetting

Consolidation theory of forgetting