Computational Models of Memory Encoding[edit]

Computational models of memory encoding have been developed in order to better understand and simulate the mostly expected, yet sometimes wildly unpredictable, behaviors of human memory. Different models have been developed for different memory tasks, which include item recognition, cued recall, free recall, and sequence memory, in an attempt to accurately explain experimentally observed behaviors.

Item Recognition[edit]

In item recognition, one is asked whether or not a given probe item has been seen before. It is important to note that the recognition of an item can include context. That is, one can be asked whether an item has been seen in a study list. So even though one may have seen the word "apple" sometime during their life, if it was not on the study list, it should not be recalled.

Item recognition can be modeled using Multiple trace theory and the attribute-similarity model.^[37] In brief, every item that one sees can be represented as a vector of the item’s attributes, which is extended by a vector representing the context at the time of encoding, and is stored in a memory matrix of all items ever seen. When a probe item is presented, the sum of the similarities to each item in the matrix (which is inversely proportional to the sum of the distances between the probe vector and each item in the memory matrix) is computed. If the similarity is above a threshold value, one would respond, "Yes, I recognize that item." Given that context continually drifts by nature of a random walk, more recently seen items, which each share a similar context vector to the context vector at the time of the recognition task, are more likely to be recognized than items seen longer ago.

Cued Recall[edit]

In cued recall, one is asked to recall the item that was paired with a given probe item. For example, one can be given a list of name-face pairs, and later be asked to recall the associated name given a face.

Cued recall can be explained by extending the attribute-similarity model used for item recognition. Because in cued recall, a wrong response can be given for a probe item, the model has to be extended accordingly to account for that. This can be achieved by adding noise to the item vectors when they are stored in the memory matrix. Furthermore, cued recall can be modeled in a probabilistic manner such that for every item stored in the memory matrix, the more similar it is to the probe item, the more likely it is to be recalled. Because the items in the memory matrix contain noise in their values, this model can account for incorrect recalls, such as mistakenly calling a person by the wrong name.

Free Recall[edit]

In free recall, one is allowed to recall items that were learned in any order. For example, you could be asked to name as many countries in Europe as you can. Free recall can be modeled using SAM (Search of Associative Memory) which is based on the dual-store model, first proposed by Atkinson and Shiffrin in 1968.^[38] SAM consists of two main components: short-term store (STS) and long-term store (LTS). In brief, when an item is seen, it is pushed into STS where it resides with other items also in STS, until it displaced and put into LTS. The longer the an item has been in STS, the more likely it is to be displaced by a new item. When items co-reside in STS, the links between those items are strengthened. Furthermore, SAM assumes that items in STS are always available for immediate recall.

SAM explains both primacy and recency effects. Probabilistically, items at the beginning of the list are more likely to remain in STS, and thus have more opportunities to strengthen their links to other items. As a result, items at the beginning of the list are made more likely to be recalled in a free-recall task (primacy effect). Because of the assumption that items in STS are always available for immediate recall, given that there were no significant distractors between learning and recall, items at the end of the list can be recalled excellently (recency effect).

Incidentally, the idea of STS and LTS was motivated by the architecture of computers, which contain short-term and long-term storage.

Sequence Memory[edit]

Sequence memory is responsible for how we remember lists of things, in which ordering matters. For example, telephone numbers are an ordered list of one digit numbers. There are currently two main computational memory models that can be applied to sequence encoding: associative chaining and positional coding.

Associative chaining theory states that every item in a list is linked to its forward and backward neighbors, with forward links being stronger than backward links, and links to closer neighbors being stronger than links to farther neighbors. For example, associative chaining predicts the tendencies of transposition errors, which occur most often with items in nearby positions. An example of a transposition error would be recalling the sequence "apple, orange, banana" instead of "apple, banana, orange."

Positional coding theory suggests that every item in a list is associated to its position in the list. For example, if the list is "apple, banana, orange, mango" apple will be associated to list position 1, banana to 2, orange to 3, and mango to 4. Furthermore, each item is also, albeit more weakly, associated to its index +/- 1, even more weakly to +/- 2, and so forth. So banana is associated not only to its actual index 2, but also to 1, 3, and 4, with varying degrees of strength. For example, positional coding can be used to explain the effects of recency and primacy. Because items at the beginning and end of a list have fewer close neighbors compared to items in the middle of the list, they have less competition for correct recall.

Although the models of associative chaining and positional coding are able to explain a great amount of behavior seen for sequence memory, they are far from perfect. For example, neither chaining nor positional coding is able to properly illustrate the details of the Ranschburg effect, which reports that sequences of items that contain repeated items are harder to reproduce than sequences of unrepeated items. Associative chaining predicts that recall of lists containing repeated items is impaired because recall of any repeated item would cue not only its true successor but also the successors of all other instances of the item. However, experimental data have shown that spaced repetition of items resulted in impaired recall of the second occurrence of the repeated item.^[39] Furthermore, it had no measurable effect on the recall of the items that followed the repeated items, contradicting the prediction of associative chaining. Positional coding predicts that repeated items will have no effect on recall, since the positions for each item in the list act as independent cues for the items, including the repeated items. That is, there is no difference between the similarity between any two items and repeated items. This, again, is not consistent with the data.

Because no comprehensive model has been defined for sequence memory to this day, it makes for an interesting area of research.

History[edit]

Encoding is still relatively new and unexplored but origins of encoding date back to age old philosophers such as Aristotle and Plato. A major figure in the history of encoding is Hermann Ebbinghaus (1850–1909). Ebbinghaus was a pioneer in the field of memory research. Using himself as a subject he studied how we learn and forget information by repeating a list of nonsense syllables to the rhythm of a metronome until they were committed to his memory.^[40] These experiments lead him to suggest the learning curve.^[40] He used these relatively meaningless words so that prior associations between meaningful words would not influence learning. He found that lists that allowed associations to be made and semantic meaning was apparent were easier to recall. Ebbinghaus’ results paved the way for experimental psychology in memory and other mental processes.

During the 1900s further progress in memory research was made. Ivan Pavlov began research pertaining to classical conditioning. His research demonstrated the ability to create a semantic relationship between two unrelated items. In 1932 Bartlett proposed the idea of mental schemas. This model proposed that whether new information would be encoded was dependent on its consistency with prior knowledge (mental schemas).^[41] This model also suggested that information not present at the time of encoding would be added to memory if it was based on schematic knowledge of the world.^[41] In this way, encoding was found to be influenced by prior knowledge. With the advance of Gestalt theory, came the realisation that memory for encoded information was often perceived as different than the stimuli that triggered it. In addition it was also influenced by the context that the stimuli were embedded in.

With advances in technology, the field of neuropsychology emerged and with it a biological basis for theories of encoding. In 1949 Hebblooked at the neuroscience aspect of encoding and stated that "neurons that fire together wire together" implying that encoding occurred as connections between neurons were established through repeated use. The 1950s and 60’s saw a shift to the information processing approach to memory based on the invention of computers, followed by the initial suggestion that encoding was the process by which information is entered into memory. At this time George Armitage Miller in 1956 wrote his paper on how our short-term memory is limited to 7 items, plus-or-minus 2 called The Magical Number Seven, Plus or Minus Two. This number was appended when studies done on chunking revealed that seven, plus or minus two could also refer to seven "packets of information". In 1974, Alan Baddeley andGraham Hitch proposed their model of working memory, which consists of the central executive, visuo-spatial sketchpad, and phonological loop as a method of encoding. In 2000, Baddeley added the episodic buffer.^[1] Simultaneously Endel Tulving (1983) proposed the idea of encoding specificity whereby context was again noted as an influence on encoding.

References[edit]

1. ^ ^{a b c d} Baddeley, A., Eysenck, M.W., & Anderson, M.C. (2009). Memory. London: Psychology Press. p. 27, 44-59
2. ^ Sperling, G. (1963). A model for visual memory tasks. Human Factors, 5, 19-31.
3. ^ Sperling, G. (1967). Successive approximations to a model for short term memory. Acta Psychologica, 27, 285-292.
4. ^ Belova, M.A., Morrison, S.E., Paton, J.J., & Salzman, C.D. (2006). The primate amygdala represents the positive and negative value of visual stimuli during learning. Nature; 439(7078): 865-870.
5. ^ Brown and Craik(2000). Missing or empty |title= (help)
6. ^ Carlson and Heth(2010). Psychology the Science of Behaviour 4e. Chapter 8: Pearson Education Canada. p. 233.
7. ^ ^{a b} Acheson, D.J., MacDonald, M.C., & Postle, B.R. (2010). The Interaction of Concreteness and Phonological Similarity in Verbal Working Memory. Journal of Experimental Psychogy: Learning, Memory and Cognition; 36:1, 17-36.
8. ^ Crawley, AP., Davis, KD., Mikulis. DJ. & Kwan, CL. (1998). Function MRI study of thalamic and cortical activation evoked by cutaneous heat, cold, and tactile stimuli. Journal of Neurophysiology: 80 (3): 1533-46
9. ^ [1]
10. ^ [2]
11. ^ ^{a b} Demb,JB., Desmond, JE., Gabrieli, JD., Glover, GH., Vaidya, CJ., & Wagner, AD. Semantic encoding and retrieval in the left inferior prefrontal cortex: a functional MRI study of task difficulty and process specificity. The Journal of Neuroscience; 15, 5870-5878.
12. ^ ^{a b c d e} Mohs, Richard C. "How Human Memory Works." 8 May 2007. HowStuffWorks.com. <http://health.howstuffworks.com/human-memory.htm> 23 February 2010.
13. ^ Schacter, D., Gilbert, D. & Wegner, D.(2011) Psychology, 2nd edition,Chapter 6: Memory, p.232
14. ^ Lepage, M., Habib, R. & Tulving. E. (1998). Hippocampal PET activations of memory encoding and retrival: The HIPER model. Hippocampus, 8:4: 313-322
15. ^ ^{a b c} Grady, CL., Horwitz, B., Haxby, JV., Maisog, JM., McIntosh, AR., Mentis, MJ., Pietrini, P., Schapiro, MB., & Underleider, LG. (1995) Age-related reductions in human recognition memory due to inpaired encoding. Science, 269:5221, 218-221.
16. ^ Birmes, P., Escande, M., Schmitt, L. & Senard, JM. (2002). Biological Factors of PTSD: neurotransmitters and neuromodulators. Encephale, 28: 241-247.
17. ^ ^{a b c} Wagner, M. (2008). The His452Tyr variant of the gene encoding the 5-HT(2a) receptor is specifically associated with consolidation of episodic memory in humans. International Journal of Neuropsychopharmacology, 11, 1163-1167.
18. ^ ^{a b c} Kandel, E. (2004). The Molecular Biology of Memory Storage: A Dialog Between Genes and Synapses. Bioscience Reports, 24, 4-5.
19. ^ Sacktor, T.C. (2008). PKMz, LTP Maintenance, and the dynamic molecular biology of memory storage. Progress in Brain Research, 169, Ch 2.
20. ^ D'Adamo, Peter J.; Peter D'Adamo; Catherine Whitney (2001). Live Right for Your Type. Penguin. ISBN 0399146733.
21. ^ ^{a b c} Cabeza, R., Daselaar, S.M., & Hongkeun, K. (2009). Overlapping brain activity between episodic memory encoding and retrieval: Roles of the task-positive and task-negative networks. Neuroimage;49: 1145-1154.
22. ^ ^{a b} Craik, F. I. M., & Watkins, M. J. (1973). The role of rehearsal in short-term memory. Journal of Verbal Learning and Verbal Behavior, 12(6), 599-607.
23. ^ Nickerson, R. S. (., & Adams, M. J. (1979). Long-term memory for a common object. Cognitive Psychology, 11(3, pp. 287-307)
24. ^ Rinck, M. (1999). Memory for everyday objects: Where are the digits on numerical keypads? Applied Cognitive Psychology, 13(4), 329-350.
25. ^ Oliphant, G. W. (1983). Repetition and recency effects in word recognition. Australian Journal of Psychology, 35(3), 393-403
26. ^ Graf, P., Mandler, G., & Haden, P. E. (1982). Simulating amnesic symptoms in normal subjects. Science, 218(4578), 1243-1244.
27. ^ Hyde, Thomas S. & Jenkins, James J. (1973). Recall for words as a function of semantic, graphic, and syntactic orienting tasks. Journal of Verbal Learning and Verbal Behavior, 12(5), 471-480
28. ^ Craik, F. I., & Tulving, E. (1975). Depth of processing and the retention of words in episodic memory. Journal of Experimental Psychology: General, 104(3), 268-294.
29. ^ Katona, G. (1940). Organizing and memorizing. New York, NY, US: Columbia University Press.
30. ^ Wiseman, S., & Neisser, U. (1974). Perceptual organization as a determinant of visual recognition memory. American Journal of Psychology, 87(4), 675-681.
31. ^ Godden, D. R., & Baddeley, A. D. (1975). Context-dependent memory in two natural environments: On land and underwater. British Journal of Psychology, 66(3), 325-331.
32. ^ Cann, A., & Ross, D. A. (1989). Olfactory stimuli as context cues in human memory. American Journal of Psychology, 102(1), 91-102.
33. ^ Smith, S. M. (1979). Remembering in and out of context. Journal of Experimental Psychology: Human Learning and Memory, 5(5), 460-471.
34. ^ Fisher, R. P., & Craik, F. I. (1977). Interaction between encoding and retrieval operations in cued recall. Journal of Experimental Psychology: Human Learning and Memory, 3(6), 701-711.
35. ^ Tulving, E. (1983). Elements of episodic memory. Oxford, England: Oxford University Press.
36. ^ ^{a b} Kanizsa, G. (1979). Organization in vision. New York: Praeger.
37. ^ Hintzman, Douglas L. & Block, Richard A. (1971) Repetition and memory: Evidence for a multiple-trace hypothesis. Journal of Experimental Psychology, 88(3), 297-306.
38. ^ Raaijmakers, J. G. W., Schiffrin, R. M. (1981). Search of associative memory. Psychological Review, 8(2), 98-134
39. ^ Crowder, R. G. (1968). Intraserial repetition effects in immediate memory. Journal of Verbal Learning and Verbal Behavior, 7, 446-451.
40. ^ ^{a b} Ebbinghaus, H. (1885). Memory: A Contribution to Experimental Psychology.
41. ^ ^{a b} Bartlett, F. C. (1932). Remembering: A study in experimental and social psychology. Cambridge, England: Cambridge University Press.

Storage (memory)

From Wikipedia, the free encyclopedia

This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (June 2007)

This section relies on references to primary sources. Please add references to secondary or tertiary sources. (April 2013)

There has been much research on whether eating prior to a cognitive recall test can effect cognitive functioning. One example was a study of the effect of breakfast timing on selected cognitive functions of elementary school students. Their results found that children who ate breakfast at school scored notably higher on most of the cognitive tests than did students who ate breakfast at home and also children who did not eat breakfast at all.^[63]

A different study was of women who were experiencing Premenstrual Syndrome. The women were either given a placebo beverage or a carbohydrate-rich beverage. The patients were tested at home, and their moods, cognitive performance, and food craving were measured before the consumption of the beverage and 30, 90, and 180 minutes after consumption. The results showed that the carbohydrate-rich beverage significantly decreased self-reported depression, anger, confusion, and carbohydrate craving 90 to 180 minutes after consumption. But more related to recall, memory word recognition also improved significantly.^[64]

Phenomena[edit]

The phenomenological account of recall is referred to as metacognition, or "knowing about knowing". This includes many states of conscious awareness known as feeling-of-knowing states, such as the tip-of-the-tongue state. It has been suggested that metacognition serves a self-regulatory purpose whereby the brain can observe errors in processing and actively devote resources to resolving the problem. It is considered an important aspect of cognition that can aid in the development of successful learning strategies that can also be generalized to other situations.^[65]

Tip-of-the-tongue[edit]

Main page: Tip of the tongue

A tip of the tongue (TOT) state refers to the perception of a large gap between the identification or knowledge of a specific subject and being able to recall descriptors or names involving said subject. This phenomena is also referred to as 'presque vu', a French term meaning "almost seen". There are two prevalent perspectives of TOT states: the psycholinguistic perspective and the metacognitive perspective.

Psycholinguistics views TOT states as a failure of retrieval from lexical memory (see Cohort Model) being cued by semantic memory (facts). Since there is an observed increase in the frequency of TOT states with age, there are two mechanisms within psycholinguistics that could account for the TOT phenomenon. The first is the degradation of lexical networks with age, where degrading connections between the priming of knowledge and vocabulary increases difficulty of successfully retrieving a word from memory. The second suggests that the culmination of knowledge, experience, and vocabulary with age results in a similar situation where many connections between a diverse vocabulary and diverse knowledge also increases the difficulty of successful retrieval of a word from memory.^[66]

The metacognitive perspective views TOT states simply as the awareness felt when such an event occurs and the perception of the experience involved. Mainly being aware of a TOT state can result in the rapid devotion of cognitive resources to resolving the state and successfully retrieving the word from memory. Such an explanation leaves much to be desired; however, the psycholinguistic perspective and the metacognitive perspective on TOT states are not mutually exclusive and both are used to observe TOT states in a laboratory setting.^[66]

An incubation effect can be observed in TOT states, where the passage of time alone can influence the resolution of the state and result in successful recall. Also, the presence of a TOT state is a good predictor that the problem can be resolved correctly, although this has been shown to occur more frequently with older-young-adults than young-adults or seniors. This is evidence for both the metacognitive perspective as well as the psycholinguistic perspective. It demonstrates the devotion of resources to searching memory, a source of cumulative information, for the desired correct information, and it also shows that we are aware of what information we know or do not know.^[67] This is why the current debate between the psycholinguistic view of TOTs as retrieval failure and the metacognitive view of TOTs as a tool for learning continues.

Similar phenomena include Déjà vu (Already seen), Jamais vu (Never Seen), and Déjà entendu (Already Heard). These occur rarely and are more prevalent in patients with traumatic head injuries, and brain disorders including epilepsy.

Involuntary memory retrieval[edit]

Often, even after years, mental states once present in consciousness return to it with apparent spontaneity and without any act of the will; that is, they are reproduced involuntarily. Here, also, in the majority of cases we at once recognise the returned mental state as one that has already been experienced; that is, we remember it. Under certain conditions, however, this accompanying consciousness is lacking, and we know only indirectly that the "now" must be identical with the "then"; yet we receive in this way a no less valid proof for its existence during the intervening time. As more exact observation teaches us, the occurrence of these involuntary reproductions is not an entirely random and accidental one. On the contrary they are brought about through the instrumentality of other immediately present mental images. Moreover they occur in certain regular ways which in general terms are described under the so-called 'laws of association'.^[68]

—Ebbinghaus, H (1885), _{as translated by Ruger & Bussenius (1913)}

Until recently, research on this phenomenon has been relatively rare, with only two types of involuntary memory retrieval identified: involuntary autobiographical memory retrieval, and involuntary semantic memory retrieval. Both of these phenomena can be considered emergent aspects of otherwise normal and quite efficient cognitive processes.

Involuntary autobiographical memory (IAM) retrieval occurs spontaneously as the result of sensory cues as well as internal cues, such as thought or intention. These cues influence us in our day-to-day lives by constantly and automatically activating unconscious memories through priming.^[69] It has been demonstrated in many studies that our specific goals and intentions will most frequently result in the retrieval of related IAM, while the second most frequent IAM retrievals result from physical cues in the surrounding context. Autobiographical memories that are unrelated to any specific cues, whether internal or external, are the least frequent to occur. It has been suggested that in this case, an error in self-regulation of memory has occurred that results in an unrelated autobiographical memory reaching the conscious mind. These findings are consistent with metacognition as the third type of experience is often identified as the most salient one.^[70]

Involuntary semantic memory retrieval (ISM), or "semantic-popping", occurs in the same fashion as IAM retrieval. However, the elicited memory is devoid of personal grounding and often considered trivial, such as a random word, image, or phrase. ISM retrieval can occur as a result of spreading activation, where words, thoughts, and concepts activate related semantic memories continually. When enough related memories are primed that an interrelated concept, word, thought, or image "pops" into consciousness and you are unaware of the extent of its relatedness within your memory. Spreading activation is thought to build over a period of many hours, days, or even weeks before a random semantic memory "pops".^[71]

False memories[edit]

Main page: False memory syndrome

False memories result from persistent beliefs, suggestions via authority figures, or statements of false information. Repeated exposure to these stimuli influence the reorganization of a person's memory, affecting its details, or implanting vivid false accounts of an event.^[72] This is usually accounted for by source-monitoring error, where a person can recall specific facts, but cannot correctly identify the source of that knowledge because of apparent loss of the association between the episodic (specific experience, or source) andsemantic (concept-based, or gist) accounts of the stored knowledge. An example of this is cryptomnesia, or inadvertent plagiarism, where one duplicates a work that they have previously encountered believing it to be their original idea.^[73] False memories can also be accounted for by the generation effect, which is an observable phenomena where repeated exposure to a belief, suggestion, or false information is better remembered with each subsequent generation. This can be seen with the misinformation effect, where an eye-witness account of an event can be influenced by a bystander account of the same event, or by suggestion via an authority figure. It is also believed to influence the recovery of repressed shocking or abusive memories in patients under hypnosis, where the recovered memory, although possibly a vivid account, could be entirely false, or have specific details influenced as the result of persistent suggestion by the therapist.^[72]

Focal retrograde amnesia[edit]

Retrograde amnesia is typically the result of physical or psychological trauma which manifests itself as the inability to remember information preceding the traumatic event. It is usually accompanied by some type of anterograde amnesia, or inability to acquire new knowledge. Focal retrograde amnesia (FRA), sometimes known as functional amnesia, refers to the presence of retrograde amnesia while knowledge acquisition remains intact (no anterograde amnesia). Memory for how to use objects and perform skills (implicit memory) may remain intact while specific knowledge of personal events or previously learned facts (explicit memory) become inaccessible or lost.^[74][75] Amnesia can result from a number of different causes, including encephalitis, severe traumatic brain injury, vitamin B₁ deficiency as seen in Korsakoff's Syndrome, and psychotic episodes, or by witnessing an emotionally traumatic event (Dissociative amnesia). Dysfunction of the temporal and frontal lobes have been observed in many cases of focal retrograde amnesia, whether metabolic or the result of lesions. However, this evidence only appears to correlate with the symptoms of retrograde amnesia as cases have been observed where patients suffering from minor concussions, showing no visible brain damage, develop FRA. It has been suggested that FRA could represent a variety of different disorders, cognitive deficits, or conditions that result in disproportionate loss of explicit memory, hence Disproportionate Retrograde Amnesia.^[75]

In popular culture[edit]

Memory phenomena are rich sources of storylines and novel situations in popular media. Two phenomena that appear regularly are total recall abilities and amnesia.

Total recall[edit]

The Argentinean author, Jorge Luis Borges wrote the short story Funes the Memorious in 1944. It depicts the life of Ireneo Funes, a fictional character who falls off his horse and experiences a head injury. After this accident, Funes has total recall abilities. He is said to recall an entire day with no mistakes, but this feat of recall takes him an entire day to accomplish. It is said that Borges was ahead of his time in his description of memory processes in this story, as it was not until the 1950s and research on the patient HM that some of what the author describes began to be understood.^[76] A more recent instance of total recall in literature is found in Dan Brown’s booksThe Da Vinci Code and Angels & Demons, in which the main character, Dr. Robert Langdon, a religious iconography and symbology professor at Harvard University, has almost total recall ability. In The Curious Incident of the Dog in the Nighttime by Mark Haddon, the main character, Christopher Boone, is a 15-year old autistic boy with total recall abilities.^[77]

Total recall is popular in television. It can be seen in Season 4 of the television show "Criminal Minds", in which the character Dr. Spencer Reid claims to have total recall ability.^[78] Agent Fox Mulder from the television show "The X-Files" has a photographic memory, a popular term for total recall.^[79] Also, the character of hospital resident Lexie Grey on the television show "Grey’s Anatomy" has total recall ability.^[80]

Amnesia[edit]

History[edit]

Memory consolidation was first referred to in the writings of the renowned Roman teacher of rhetoric Quintillian. He noted the “curious fact… that the interval of a single night will greatly increase the strength of the memory,” and presented the possibility that “… the power of recollection .. undergoes a process of ripening and maturing during the time which intervenes.” The process of consolidation was later proposed based on clinical data illustrated in 1882 by Ribot’s Law of Regression, “progressive destruction advances progressively from the unstable to the stable”. This idea was elaborated on by William H. Burnham a few years later in a paper on amnesia integrating findings from experimental psychology and neurology. Coining of the term “consolidation” is credited to the German researchers Müller and Alfons Pilzecker who rediscovered the concept that memory takes time to fixate or undergo “Konsolidierung” in their studies conducted between 1892 and 1900.^[1] The two proposed the perseveration-consolidation hypothesis after they found that new information learned could disrupt information previously learnt if not enough time had passed to allow the old information to be consolidated.^[2] This led to the suggestion that new memories are fragile in nature but as time passes they become solidified.^[2]

Systematic studies of retrograde amnesia started to emerge in the 1960s and 1970s. The case of Henry Molaison, formerly known as patient H.M., became a landmark in studies of memory as it relates to amnesia and the removal of the hippocampal zone and sparked massive interest in the study of brain lesions and their effect on memory. After Molaison underwent a bilateral medial temporal loberesection to alleviate epileptic symptoms the patient began to suffer from memory impairments. Molaison lost the ability to encode and consolidate newly learned information leading researchers to conclude the medial temporal lobe (MTL) was an important structureinvolved in this process.^[3] Molaison also showed signs of retrograde amnesia spanning a period of about 3 years prior to the surgerysuggesting that recently acquired memories of as long as a couple years could remain in the MTL prior to consolidation into other brain areas.^[4] Research into other patients with resections of the MTL have shown a positive relationship between the degree of memory impairment and the extent of MTL removal which points to a temporal gradient in the consolidating nature of the MTL.^[3]

These studies were accompanied by the creation of animal models of human amnesia in an effort to identify brain substrates critical for slow consolidation. Meanwhile, neuropharmacological studies of selected brain areas began to shed light on the molecules possibly responsible for fast consolidation.^[1] In recent decades, advancements in cellular preparations, molecular biology, and neurogenetics have revolutionized the study of consolidation. Providing additional support is the study of functional brain activity in humans which has revealed that the activity of brain regions changes over time after a new memory is acquired.^[3] This change can occur as quickly as a couple hours after the memory has been encoded suggesting that there is a temporal dimension to the reorganization of the memory as it is represented in the brain.^[2]

Synaptic consolidation[edit]

Synaptic consolidation is one form of memory consolidation seen across all species and long-term memory tasks. Long-term memory, when discussed in the arena of synaptic consolidation, is memory that lasts for at least 24 hours. An exception to this 24-hour rule islong-term potentiation, or LTP, a model of synaptic plasticity related to learning, in which an hour is thought to be sufficient. Synaptic consolidation is achieved faster than systems consolidation, within only minutes to hours of learning.^[1] LTP, one of the best understood forms of synaptic plasticity, is thought to be a possible underlying process in synaptic consolidation.

Standard Model[edit]

The standard model of synaptic consolidation suggests that alterations of synaptic protein synthesis and changes in membrane potential are achieved through activatingintracellular transduction cascades. These molecular cascades trigger transcription factors that lead to changes in gene expression. The result of the gene expression is the lasting alteration of synaptic proteins, as well as synaptic remodeling and growth. In a short time-frame immediately following learning, the molecular cascade, expression and process of both transcription factors and immediate early genes, are susceptible to disruptions. Disruptions caused by specific drugs, antibodies and gross physical trauma can block the effects of synaptic consolidation.^[1]

Long-term potentiation[edit]

LTP can be thought of as the prolonged strengthening of synaptic transmission,^[5] and is known to produce increases in the neurotransmitter production and receptor sensitivity, lasting minutes to even days. The process of LTP is regarded as a contributing factor to synaptic plasticity and in the growth of synaptic strength, which are suggested to underlie memory formation. LTP is also considered to be an important mechanism in terms of maintaining memories within brain regions,^[6] and therefore is thought to be involved in learning.^[5] There is compelling evidence that LTP is critical for Pavlovian fear conditioning in rats suggesting that it mediates learning and memory in mammals. Specifically, NMDA-receptor antagonists appear to block the induction of both LTP and fear conditioning and that fear conditioning increases amygdaloidal synaptic transmission that would result in LTP.^[7]

Timeline of consolidation[edit]

Synaptic consolidation, when compared to systems consolidation (which is said to take weeks to months to years to be accomplished), is considerably faster. There is evidence to suggest that synaptic consolidation takes place within minutes to hours of memory encoding or learning, and as such is considered the ‘fast’ type of consolidation.^[1] As soon as six hours after training, memories become impervious to interferences that disrupt synaptic consolidation and the formation of long-term memory.

Spacing effect[edit]

Distributed learning has been found to enhance memory consolidation, specifically for relational memory. Experimental results suggest that distributing learning over the course of 24 hours decreases the rate of forgetting compared to massed learning, and enhances relational memory consolidation. When interpreted in the context of synaptic consolidation, mechanisms of synaptic strengthening may depend on the spacing of memory reactivation to allow sufficient time for protein synthesis to occur, and thereby strengthen long-term memory.^[8]

Protein synthesis[edit]

Protein synthesis plays an important role in the formation of new memories. Studies have shown that protein synthesis inhibitors administered after learning, weaken memory, suggesting that protein synthesis is required for memory consolidation. Additionally, reports have suggested that the effects of protein synthesis inhibitors also inhibit LTP.^[9]However, it should be noted that other results have shown that protein synthesis may not in fact be necessary for memory consolidation, as it has been found that the formation of memories can withstand vast amounts of protein synthesis inhibition, suggesting that this criterion of protein synthesis as necessary for memory consolidation is not unconditional.^[9]

Dietary flavonoids[edit]

There is evidence to suggest that dietary flavonoids have effects on encouraging LTP and synaptic plasticity, therefore affecting memory. Specifically, it was found that dietary-derived flavonoids might protect neurons, enhance neuronal function, and stimulate neuronal regeneration. Additionally, these dietary phytochemicals interact with several neuronalsignaling cascade pathways that are responsible for alterations in LTP, and consequently, learning and human memory.^[6] Flavonoids may trigger certain events, including the activation of the CREB transcription factor, which is important to the enhancement of short-term and long-term memory. This activation then triggers the synthesis of important proteins related to LTP, ultimately leading to synapse growth and eventually long-term memory.^[6]

Systems consolidation[edit]

Systems Consolidation is the second form of memory consolidation. It is a reorganization process in which memories from the hippocampal region, where memories are firstencoded, are moved to the neo-cortex in a more permanent form of storage.^[10] Systems consolidation is a slow dynamic process that can take from one to two decades to be fully formed in humans, unlike synaptic consolidation that only takes minutes to hours for new information to stabilize into memories.^[10]

Standard Model[edit]

The Standard model of systems consolidation has been summarized by Squire and Alvarez (1995);^[11] it states that when novel information is originally encoded and registered, memory of these new stimuli becomes retained in both the hippocampus and cortical regions.^[12] Later the hippocampus’ representations of this information become active inexplicit (conscious) recall or implicit (unconscious) recall like in sleep and ‘offline’ processes.^[1]

Memory is retained in the hippocampus for up to one week after initial learning, representing the hippocampus-dependent stage.^[12] During this stage the hippocampus is ‘teaching’ the cortex more and more about the information and when the information is recalled it strengthens the cortico-cortical connection thus making the memory hippocampus-independent.^[1] Therefore from one week and beyond the initial training experience, the memory is slowly transferred to the neo-cortex where it becomes permanently stored.^[1] In this view the hippocampus can perform the task of storing memories temporarily because the synapses are able to change quickly whereas the neocortical synapses change over time.^[11] Consolidation is thus the process whereby the hippocampus activates the neocortex continually leading to strong connections between the two. Since the hippocampus can only support memories temporarily the remaining activation will be seen only in the neocortex which is able to support memory indefinitely. Squire and Alvarez took the temporally graded nature of patients with retrograde amnesia as support for the notion that once a connection has been established within the neocortex the hippocampus is no longer required, but this process is dynamic and extends for several years.

Squire and Alvarez also proposed the idea that MTL structures play a role in the consolidation of memories within the neocortex by providing a binding area for multiple corticalregions involved in the initial encoding of the memory.^[11] In this sense the MTL would act as a relay station for the various perceptual input that make up a memory and stores it as a whole event. After this has occurred the MTL directs information towards the neocortex to provide a permanent representation of the memory.

Multiple trace theory[edit]

Multiple Trace Theory (MTT) builds on the distinction between semantic memory and episodic memory and addresses perceived shortcomings of the standard model with respect to the dependency of the hippocampus. Multiple Trace Theory argues that the hippocampus is always involved in the retrieval and storage of episodic memories.^[13] It is thought that semantic memories, including basic information encoded during the storage of episodic memories, can be established in structures apart from the hippocampal system such as the neo-cortex in the process of consolidation.^[13] Hence, while proper hippocampal functioning is necessary for the retention and retrieval of episodic memories, it is less necessary during the encoding and use of semantic memories. As memories age there are long-term interactions between the hippocampus and neo-cortex and this leads to the establishment of aspects of memory within structures aside from the hippocampus.^[13] MTT thus states that both episodic and semantic memories rely on the hippocampus and the latter becomes somewhat independent of the hippocampus during consolidation.^[13] An important distinction between MTT and the standard model is that the standard model proposes that all memories become independent of the hippocampus after several years. However, Nadel and Moscovitch have shown that the hippocampus was involved in memory recall for all remote autobiographical memories no matter of their age.^[13] An important point they make while interpreting the results is that activation in the hippocampus was equally as strong regardless of the fact that the memories recalled were as old as 45 years prior to the date of the experiment.^[13] This is complicated by the fact that the hippocampus is constantly involved in the encoding of new events and activation due to this fact is hard to separate using baseline measures.^[13] Because of this, activation of the hippocampus during retrieval of distant memories may simply be a by-product of the subject encoding the study as an event.^[13]

Criticisms of multiple trace theory[edit]

Haist, Gore, and Mao, sought to examine the temporal nature of consolidation within the hippocampus to test the multiple trace theory against the standard view.^[14] They found that the hippocampus does not substantially contribute to the recollection of remote memories after a period of a few years. They claim that advances in the functional magnetic resonance imaging have allowed them to improve their distinction between the hippocampus and the entorhinal cortex which they claim is more enduring in its activation from remote memory retrieval.^[14] They also criticize the use of memories during testing which cannot be confirmed as accurate.^[14] Finally, they state that the initial interview in the scanner acted as an encoding event as such differences between recent and remote memories would be obscured.^[14]

Semantic vs. episodic memory[edit]

Nadel and Moscovitch argued that when studying the structures and systems involved in memory consolidation, semantic memory and episodic memory need to be distinguished as relying on two different memory systems. When episodic information is encoded there are semantic aspects of the memory that are encoded as well and this is proposed as an explanation of the varying gradients of memory loss seen in amnesic patients.^[13] Amnesic patients with hippocampal damage show traces of memories and this has been used as support for the standard model because it suggests that memories are retained apart from the hippocampal system.^[13] Nadel and Mocovitch argue that these retained memories have lost the richness of experience and exist as depersonalized events that have been semanticized over time.^[13] They suggest that this instead provides support for their notion that episodic memories rely significantly on the hippocampal system but semantic memories can be established elsewhere in the brain and survive hippocampal damage.^[13]

Declarative vs. procedural knowledge consolidation[edit]

Learning can be distinguished by two forms of knowledge: declarative and procedural. Declarative information includes the conscious recall of facts, episodes, and lists, and its storage typically connected with the MTL and the hippocampal systems as it includes the encoding of both semantic and episodic information of events. Procedural knowledge however has been said to function separate from this system as it relies primarily on motor areas of the brain.^[15] The implicit nature of procedural knowledge allows it to exist absent from the conscious awareness that the information is there. Amnesic patients have shown retained ability to be trained on tasks and exhibit learning without the subject being aware that the training had ever taken place.^[15] This introduces a dissociation between the two forms of memory and the fact that one form can exist absent the other suggests separate mechanisms are involved in consolidation. Squire has proposed the procedural knowledge is consolidated in some cases by the extrapyramidal motor system.^[15] Squire demonstrated that intact learning of certain motor, perceptual, and cognitive skills can be retained in patients with amnesia.^[15] They also retain the ability to be influenced by priming effects without the patients being able to consciously recall any training session occurring.^[15]

Emotional and stressful memory consolidation[edit]

The amygdala, specifically the basolateral region (BLA) is involved in the encoding of significant experiences and has been directly linked to memorable events.^[2] Extensive evidence suggests that stress hormones such as epinephrine play a critical role in consolidating new memories and this is why stressful memories are recalled vividly.^[16] Studies by Gold and van Buskirk provided initial evidence for this relationship when they showed that injections of epinephrine into subjects following a training period resulted in greater long-term retention of task related memories.^[9][17] This study also provided evidence that the level of epinephrine injected was related to the level of retention suggesting that the level of stress or emotionality of the memory plays a role on the level of retention. It is suggested that epinephrine affects memory consolidation by activating the amygdala and studies have shown that antagonism of beta-andrenoreceptors prior to injection of epinephrine will block the retention of memory effects seen previously.^[18][19] This is supported by the fact that beta-adrenoreceptor agonists have the opposite effect on the enhancement of memory consolidation.^[18][19] The BLA is thought to be actively involved in memory consolidation and is influenced strongly by stress hormones resulting in increased activation and as such increased memory retention.^[16] The BLA then projects to the hippocampus resulting in a strengthened memory.^[2] This relationship was studied by Packard and Chen who found that when glutamate was administered to the hippocampus, enhanced consolidation was seen during food-rewarded maze tasks.^[20] The opposite effect was also seen when the amygdala was inactivated using lidocane.^[20] Studies appear to suggest that the amygdala effects the consolidation of memories through its influence with stress hormones and the projections to other brain areas implicated in memory consolidation.^[2]

Sleep consolidation[edit]

See also: Sleep and Memory

Rapid eye movement (REM) sleep has been thought of to be an important concept in the overnight learning in humans by establishing information in the hippocampal and corticalregions of the brain.^[21] REM sleep elicits an increase in neuronal activity following an enriched or novel waking experience, thus increasing neuronal plasticity and therefore playing an essential role in the consolidation of memories.^[22] This has come into question in recent years however and studies on sleep deprivation have shown that animals and humans who are denied REM sleep do not show deficits in task learning. It has been proposed that since the brain is in a non-memory encoding state during sleep consolidation would be unlikely to occur.^[23]

Recent studies have examined the relationship between REM sleep and procedural learning consolidation. In particular studies have been done on sensory and motor related tasks. In one study testing finger-tapping, people were split into two groups and tested post-training with or without intervening sleep; results concluded that sleep post-training increases both speed and accuracy in this particular task, while increasing the activation of both cortical and hippocampal regions; whereas the post-training awake group had no such improvements.^[21] It has been theorized that this may be related more-so to a process of synaptic consolidation rather than systems consolidation because of the short-term nature of the process involved.^[23] Researchers examining the effect of sleep on motor learning have noted that while consolidation occurs over a period of 4–6 hours during sleep, this is also true during waking hours, which may negate any role of sleep in learning.^[23] In this sense sleep would serve no special purpose to enhance consolidation of memories because it occurs independently of sleep. Other studies have examined the process of replay which has been described as a reactivation of patterns that were stimulated during a learning phase. Replay has been demonstrated in the hippocampus and this has lent support to the notion that it serves a consolidation purpose.^[23] However, replay is not specific to sleep and both rats and primates show signs during restful-awake periods.^[23] Also, replay may simply be residual activation in areas that were involved previously in the learning phase and may have no actual effect on consolidation.^[23] This reactivation of the memory traces has also been seen in non-REM sleep specifically for hippocampus-dependant memories.^[24] Researchers have noted strong reactivation of the hippocampus during sleep immediately after a learning task. This reactivation led to enhanced performance on the learned task.^[24] Researchers following this line of work have come to assume that dreams are a by-product of the reactivation of the brain areas and this can explain why dreams may be unrelated to the information being consolidated.^[24] The dream experience itself is not what enhances memory performance but rather it is the reactivation of the neural circuits that causes this.

Zif268 & REM Sleep[edit]

Zif268 is an Immediate Early Gene (IEG) thought to be involved in neuroplasticity by an up-regulation of the transcription factor during REM sleep after pre-exposure to an enriched environment.^[22] Results from studies testing the effects of zif268 on mice brains postmortem, suggest that a waking experience prior to sleep can have an enduring effect in the brain, due to an increase of neuroplasticity.^[22]

Reconsolidation[edit]

Memory reconsolidation is the process of previously consolidated memories being recalled and actively consolidated.^[5] It is a distinct process that serves to maintain, strengthen and modify memories that are already stored in the long-term memory. Once memories undergo the process of consolidation and become part of long-term memory, they are thought of as stable. However, the retrieval of a memory trace can cause another labile phase that then requires an active process to make the memory stable after retrieval is complete.^[5] It is believed that post-retrieval stabilization is different and distinct from consolidation, despite its overlap in function (e.g. storage) and its mechanisms (e.g. protein synthesis). Memory modification needs to be demonstrated in the retrieval in order for this independent process to be valid.^[5]

History[edit]

The theory of reconsolidation has been debated for many years and has become quite controversial. Reconsolidation was first conceptualized after studies were done on elimination of phobias with electroconvulsive shock therapy; the disruption of the consolidated fear memory after shock administration led to further investigation into the concept.^[5] In many early studies electroconvulsive shock therapy was used to test for reconsolidation, as it was a known amnesic agent, and lead to memory loss if administered directly after the retrieval of a memory.^[1] Later research using Pavlovian fear conditioning on rats found that a consolidated fear memory can return to a labile state, with immediate amygdalainfusions of the protein synthesis inhibitor anisomycin, but not infusions made six hours afterwards.^[25] It was concluded that consolidated fear memory, when reactivated, enters a changeable state that requires de novo protein synthesis for new consolidation or reconsolidation of the old memory.^[25] In addition to fear memories, appetitive memories are also prone to reconsolidation episodes, which can be disrupted likewise after local administration of a protein activity inhibitor.^[26] Since these break through studies many more have been done testing the theory of reconsolidation. Studies have been done on numerous subjects including; crabs, chicks, honeybees, medaka fish, lymnaea, humans and rodents.^[5]

Criticisms[edit]

Some studies have supported this theory, while others have failed to demonstrate disruption of consolidated memory after retrieval. It is important to note that negative results may be examples of conditions where memories are not susceptible to a permanent disruption, thus a determining factor of reconsolidation.^[5] After much debate and a detailed review of this field it had been concluded that reconsolidation was a real phenomenon.^[27] More recently Tronson and Taylor compiled a lengthy summary of multiple reconsolidation studies, noting a number of studies were unable to show memory impairments due to blocked reconsolidation. However the need for standardized methods was underscored as in some learning tasks such as fear conditioning, certain forms of memory reactivation could actually represent new extinction learning rather than activation of an old memory trace. Under this possibility, traditional disruptions of reconsolidation might actually maintain the original memory trace but preventing the consolidation of extinction learning.^[5]

Reconsolidation experiments are more difficult to run than typical consolidation experiments as disruption of a previously consolidated memory must be shown to be specific to the reactivation of the original memory trace. Furthermore, it is important to demonstrate that the vulnerability of reactivation occurs in a limited time frame, which can be assessed by delaying infusion till six hours after reactivation. It is also useful to show that the behavioral measure used to assess disruption of memory is not just due to task impairment caused by the procedure, which can be demonstrated by testing control groups in absence of the original learning. Finally, it is important to rule out alternative explanations, such asextinction learning by lengthening the reactivation phase.^[5]

Distinctions from consolidation[edit]

Questions arose if reconsolidation was a unique process or merely another phase of consolidation. Both consolidation and reconsolidation can be disrupted by pharmacological agents (e.g. the protein synthesis inhibitor anisomycin) and both require the transcription factor CREB. However, recent amygdala research suggests that BDNF is required for consolidation (but not reconsolidation) whereas the transcription factor and immediate early gene Zif268 is required for reconsolidation but not consolidation.^[28] A similar double dissociation between Zif268 for reconsolidation and BDNF for consolidation was found in the hippocampus for fear conditioning.^[29] However not all memory tasks show this double dissociation, such as object recognition memory.^[30]

See also[edit]

• Atkinson-Shiffrin memory model
• Coherence therapy
• Engram
• Patient HM
• Multiple trace theory

References[edit]

1. ^ ^{a b c d e f g h i j} Dudai, Y. (2004). "The Neurobiology of Consolidations, Or, How Stable is the Engram?". Annual Review of Psychology 55: 51–86.doi:10.1146/annurev.psych.55.090902.142050. PMID 14744210. edit
2. ^ ^{a b c d e f} McGaugh, J. L. (2000). "Memory--a Century of Consolidation". Science 287(5451): 248–251. doi:10.1126/science.287.5451.248. PMID 10634773. edit
3. ^ ^{a b c} Scoville, W. B.; Milner, B. (1957). "Loss of Recent Memory After Bilateral Hippocampal Lesions". Journal of Neurology, Neurosurgery & Psychiatry 20 (1): 11–21. doi:10.1136/jnnp.20.1.11. PMC 497229. PMID 13406589. edit
4. ^ Milner, B.; Corkin, S.; Teuber, H. -L. (1968). "Further analysis of the hippocampal amnesic syndrome: 14-year follow-up study of H.M". Neuropsychologia 6 (3): 215.doi:10.1016/0028-3932(68)90021-3. edit
5. ^ ^{a b c d e f g h i j} Tronson, N. C.; Taylor, J. R. (2007). "Molecular mechanisms of memory reconsolidation". Nature Reviews Neuroscience 8 (4): 262–275.doi:10.1038/nrn2090. PMID 17342174. edit
6. ^ ^{a b c} Spencer, J. P. E. (2008). "Food for thought: The role of dietary flavonoids in enhancing human memory, learning and neuro-cognitive performance". Proceedings of the Nutrition Society 67 (2): 238–252. doi:10.1017/S0029665108007088.PMID 18412998. edit
7. ^ Maren, S. (1999). "Long-term potentiation in the amygdala: A mechanism for emotional learning and memory". Trends in Neurosciences 22 (12): 561–567.doi:10.1016/S0166-2236(99)01465-4. PMID 10542437. edit
8. ^ Litman, L. & Davachi, L. (2008). Distributed learning enhances relational memory consolidation. Learn. Mem., 15, 711-716.
9. ^ ^{a b c} Gold, P. E. (2008). "Protein synthesis inhibition and memory: Formation vs amnesia". Neurobiology of Learning and Memory 89 (3): 201–211.doi:10.1016/j.nlm.2007.10.006. PMC 2346577. PMID 18054504. edit
10. ^ ^{a b} Roediger, H. L., Dudai, Y., & Fitzpatrick, S. M. (2007). Science of memory: concepts. New York, NY: Oxford University Press.
11. ^ ^{a b c} Squire, L. R.; Alvarez, P. (1995). "Retrograde amnesia and memory consolidation: A neurobiological perspective". Current Opinion in Neurobiology 5 (2): 169–177. doi:10.1016/0959-4388(95)80023-9. PMID 7620304. edit
12. ^ ^{a b} Frankland, P. W.; Bontempi, B. (2005). "The organization of recent and remote memories". Nature Reviews Neuroscience 6 (2): 119–130. doi:10.1038/nrn1607.PMID 15685217. edit
13. ^ ^{a b c d e f g h i j k l} Nadel, L.; Moscovitch, M. (1997). "Memory consolidation, retrograde amnesia and the hippocampal complex". Current Opinion in Neurobiology 7 (2): 217–227. doi:10.1016/S0959-4388(97)80010-4. PMID 9142752. edit
14. ^ ^{a b c d} Haist, F.; Gore, J. B.; Mao, H. (2001). "Consolidation of human memory over decades revealed by functional magnetic resonance imaging". Nature Neuroscience 4(11): 1139–1145. doi:10.1038/nn739. PMID 11600889. edit
15. ^ ^{a b c d e} Squire, L. R. (1986). "Mechanisms of memory". Science 232 (4758): 1612–1619. doi:10.1126/science.3086978. PMID 3086978. edit
16. ^ ^{a b} McGaugh, J. L.; Roozendaal, B. (2002). "Role of adrenal stress hormones in forming lasting memories in the brain". Current Opinion in Neurobiology 12 (2): 205–210. doi:10.1016/S0959-4388(02)00306-9. PMID 12015238. edit
17. ^ Gold, P. E.; McIntyre, C.; McNay, E.; Stefani, M.; Korol, D. L. (2001). "Neurochemical referees of dueling memory systems.". Memory consolidation: Essays in honor of James L. McGaugh. p. 219. doi:10.1037/10413-012. ISBN 1-55798-783-1. edit
18. ^ ^{a b} "Modulating effects of posttraining epinephrine on memory: involvement of the amygdala noradrenergic system". Brain Res. 368 (1): 125–33. March 1986.doi:10.1016/0006-8993(86)91049-8. PMID 3955350.
19. ^ ^{a b} "Involvement of amygdala pathways in the influence of post-training intra-amygdala norepinephrine and peripheral epinephrine on memory storage". Brain Res. 508 (2): 225–33. February 1990. doi:10.1016/0006-8993(90)90400-6. PMID 2306613.
20. ^ ^{a b} Packard, Mark G; Chen, Scott A (September 1999). "The basolateral amygdala is a cofactor in memory enhancement produced by intrahippocampal glutamate injections".Psychobiology 27 (3): 377–385.
21. ^ ^{a b} Walker, M.P.; Stickgold, R.; Alsop, D.; Gaab, N.; Schlaug, G. (2005). "Sleep-dependent motor memory plasticity in the human brain". Neuroscience 133: 911–917.
22. ^ ^{a b c} Ribeiro, S. (1999). "Brain Gene Expression During REM Sleep Depends on Prior Waking Experience". Learning & Memory 6 (5): 500–510. doi:10.1101/lm.6.5.500. edit
23. ^ ^{a b c d e f} Vertes, R. P. (2004). "Memory Consolidation in Sleep". Neuron 44 (1): 135–148. doi:10.1016/j.neuron.2004.08.034. PMID 15450166. edit
24. ^ ^{a b c} Wamsley, E. J.; Tucker, M.; Payne, J. D.; Benavides, J. A.; Stickgold, R. (2010)."Dreaming of a Learning Task is Associated with Enhanced Sleep-Dependent Memory Consolidation". Current Biology 20 (9): 850–855. doi:10.1016/j.cub.2010.03.027.PMC 2869395. PMID 20417102. edit
25. ^ ^{a b} Nader, K., Schafe, G. E. & LeDoux, J. E. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature 406, 722–726 (2000).
26. ^ Crespo, J.A.; Stöckl, P., Ueberall, F., Marcel, J., Saria, A. & Zernig, G. (February 2012)."Activation of PKCzeta and PKMzeta in the nucleus accumbens core is necessary for the retrieval, consolidation and reconsolidation of the drug memory". PLoS ONE. Retrieved 17 March 2012.
27. ^ Sara SJ. 2000. Retrieval and reconsolidation: toward a neurobiology of remembering. Learn. Mem. 7:73–84
28. ^ Debiec, J., Doyere, V., Nader, K., LeDoux, J.E. (February 28, 2006). Directly reactivated, but not indirectly reactivated, memories undergo reconsolidation in the amygdala. PNAS, Volume 103, Number 9, 3428-3433.
29. ^ Lee, J. L.; Everitt, B. J.; Thomas, K. L. (2004). "Independent cellular processes for hippocampal memory consolidation and reconsolidation". Science 304: 839–843.
30. ^ Bozon, B.; Davis, S.; Laroche, S. (2003). "A requirement for the immediate early gene zif268 in reconsolidation of recognition memory after retrieval". Neuron 40: 695–701.