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Autor     Jonathan L. C. Lee
Titel    Reconsolidation: maintaining memory relevance
Zeitschrift    Trends in Neurosciences
Datum    August 2009
Jahrgang    32
Nummer    8
Seiten    413-420
Anmerkung    This paper has been published after the submission of Jm's thesis. However, the paper is listed in the bibliography and is mentioned in the text of the thesis (e.g. page 44), such that one can assume that the author had a version of the paper available while finalising the thesis. Note also that the linked version of the paper has a page count from 1-16, which is also used for the documentation here.
DOI    10.1016/j.tins.2009.05.002
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650827/pdf/emss-53055.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    10


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The search for an endogenous function for the process of reconsolidation remains a fundamental issue. As noted by Dudai (2007), reconsolidation might not serve any function, particularly given the remote chance of encountering in everyday life the forms of agents used experimentally to induce amnesia. Nevertheless, interference is a potent cause of amnesia in reconsolidation studies (e.g., Walker et al., 2003; Hupbach et al., 2007) and stress can also be detrimental to reactivated memories (Maroun & Akirav, 2008; Wang et al., 2008), thereby suggesting that retrieval-induced plasticity places a memory trace at risk of disruption. As such, reconsolidation has been conceptualized as a fundamental process in the ongoing modification and storage of memories.

Indeed, it has often been suggested that reconsolidation might enable memories to be modified or updated (e.g., Tronson & Taylor, 2007; Dudai & Eisenberg, 2004; Sara, 2000). Generally, memories are retrieved in circumstances wherein additional complementary information is presented. As such, the capacity for plastic alterations in memory strength or content following memory retrieval would appear adaptive in terms of maintaining a memory’s relevance with respect to guiding future behaviour (Lee, 2009). Indeed, in terms of human episodic memories, interference congruent with retrieval of a prior memory results in an incorrectly updated memory for a list of items (Hupbach et al., 2007), thereby suggesting a role of reconsolidation in updating memories. However, Tronel and colleagues (2005), in a study adopting inhibitory avoidance learning in rats, did not find evidence that [reconsolidation is functionally involved in linking new information to a reactivated memory.]

[page 2]

While much has been learned regarding the mechanisms of reconsolidation, the search for an endogenous function of the process remains a fundamental issue. As noted by Dudai [11], reconsolidation might not serve any function, especially given the remote chance of encountering in real life the kinds of agents used experimentally to induce amnesia. Nevertheless, interference is a potent cause of amnesia in reconsolidation studies [12-14], and stress can also be detrimental to reactivated memories [15, 16], suggesting that retrieval-induced plasticity does place a memory genuinely at risk of disruption.

It has often been suggested that reconsolidation may enable memories to be modified or updated [5, 8, 9, 13, 17, 18]. Memories are retrieved often in situations presenting additional complementary information. Thus the capacity for plastic changes in memory strength or content following memory retrieval seems potentially adaptive in terms of maintaining a memory’s relevance in guiding future behaviour. [Three studies are of direct relevance to the hypothesis that reconsolidation mediates memory updating (see Box 1 for brief experimental details of the following tasks).] Firstly, in human episodic memories, interference congruent with retrieval of a prior memory results in an incorrectly updated memory for a list of items [13]. This finding is consistent with, though not directly demonstrative of, a role of reconsolidation in updating memories. Moreover, a prior study of inhibitory avoidance learning in rats did not provide evidence that reconsolidation is functionally involved in linking new information to a reactivated memory [19].

[page 6]

Thus reconsolidation may be viewed as a fundamental process in the ongoing modification and storage of memories.


5. Tronson NC, Taylor JR. Molecular mechanisms of memory reconsolidation. Nat Rev Neurosci. 2007; 8:262–275. [PubMed: 17342174]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

9. Sara SJ. Retrieval and reconsolidation: Toward a neurobiology of remembering. Learn Mem. 2000; 7:73–84. [PubMed: 10753974]

11. Dudai, Y. Post-activation state: a critical rite of passage of memories. In: Bontempi, B., et al., editors. Memories: Molecules and Circuits. Springer-Verlag; 2007. p. 69-82.

12. Walker MP, et al. Dissociable stages of human memory consolidation and reconsolidation. Nature. 2003; 425:616–620. [PubMed: 14534587]

13. Hupbach A, et al. Reconsolidation of episodic memories: A subtle reminder triggers integration of new information. Learn Mem. 2007; 14:47–53. [PubMed: 17202429]

14. Gordon WC, Feldman DT. Reactivation-induced interference in a short-term retention paradigm. Learn Motiv. 1978; 9:164–178.

15. Maroun M, Akirav I. Arousal and stress effects on consolidation and reconsolidation of recognition memory. Neuropsychopharmacology. 2008; 33:394–405. [PubMed: 17429409]

16. Wang XY, et al. Stress impairs reconsolidation of drug memory via glucocorticoid receptors in the basolateral amygdala. J Neurosci. 2008; 28:5602–5610. [PubMed: 18495894]

17. Dudai Y. The neurobiology of consolidations, or, how stable is the engram? Annu Rev Psychol. 2004; 55:51–86. [PubMed: 14744210]

18. Dudai Y. Reconsolidation: the advantage of being refocused. Curr Opin Neurobiol. 2006; 16:174– 178. [PubMed: 16563730]

19. Tronel S, et al. Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS Biol. 2005; 3:e293. [PubMed: 16104829]

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[However, Tronel and colleagues (2005), in a study adopting inhibitory avoidance learning in rats, did not find evidence that] reconsolidation is functionally involved in linking new information to a reactivated memory. Using the doubly dissociable mechanisms of inhibitory avoidance memory consolidation and reconsolidation, these researchers demonstrated that second-order conditioning recruited consolidation processes in a selective manner. However, according to Tronson and Taylor (2007), linking new information to an old memory can be conceptualized as new learning based upon evoked memories, which would be expected to necessitate consolidation mechanisms rather than true memory updating. Lee (2008) recently directly addressed the functional role of memory reconsolidation employing the doubly dissociable mechanisms of consolidation and reconsolidation in hippocampal contextual fear memories, finding that a basic form of memory updating, namely strengthening through a further learning episode, was selectively dependent upon reconsolidation mechanisms. Thus, as suggested by Lee(2009), memory reconsolidation might prove to be the mechanism by which memories are updated through further experience, although it remains to be determined whether reconsolidation has a similar functional role in other forms of memory updating, such as memory weakening or changes in memory content.

Although the mechanisms of memory reconsolidation largely recapitulate those of initial consolidation, there are notable dissociations between the two (see Moore & Roche, 2007 and Alberini, 2005 for a comprehensive review). In particular, there is evidence that reconsolidation recruits specific mechanisms that are not crucially involved in consolidation. The reconsolidation, but not consolidation, of discrete fear memories is vulnerable to ßadrenoceptor blockade (Debiec & LeDoux, 2004). Moreover, the cellular mechanisms of memory consolidation and reconsolidation for both contextual fear (Lee et al., 2004) and inhibitory avoidance (Taubenfeld et al., 2001; Milekic et al., 2007) are doubly dissociable. As such, reconsolidation is a neurobiologically distinct memory process, which is [increasingly associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 (Lee et al., 2004, 2005).]

[page 2]

Moreover, a prior study of inhibitory avoidance learning in rats did not provide evidence that reconsolidation is functionally involved in linking new information to a reactivated memory [19]. Using the doubly dissociable mechanisms of inhibitory avoidance memory consolidation and reconsolidation, Tronel et al. showed that second-order conditioning recruited consolidation processes selectively [19]. However, linking new information to an old memory can be viewed simply as new learning based upon evoked memories, which would be expected to necessitate consolidation mechanisms, rather than true memory updating [5]. In a study designed to address directly the functional role of memory reconsolidation, I similarly capitalised on the doubly dissociable mechanisms of consolidation and reconsolidation in hippocampal contextual fear memories. A simple form of memory updating, namely strengthening through a further learning episode, was dependent selectively upon reconsolidation mechanisms [20]. Therefore, memory reconsolidation may well prove to be the mechanism by which memories are updated through further experience, though it remains to be determined whether reconsolidation plays a similar functional role in other forms of memory updating, such as memory weakening or changes in memory content.

[page 3]

Indeed, although the mechanisms of memory reconsolidation largely recapitulate those of initial consolidation, there are notable dissociations between the two (See Alberini, 2005 [6] for a comprehensive review). In particular, there is evidence that reconsolidation recruits specific mechanisms that are not critically involved in consolidation. The reconsolidation, but not consolidation, of discrete fear memories is vulnerable to β-adrenergic receptor blockade [21]. Moreover, the cellular mechanisms of memory consolidation and reconsolidation for both contextual fear [22] and inhibitory avoidance [23, 24] are doubly dissociable. [Such double dissociations rule out simple quantitative or non-specific factors, such as time or the absence of the highly motivating footshock reinforcer, as being the cause of differences between the mechamisms of consolidation and reconsolidation.] Therefore, reconsolidation is a neurobiologically-distinct memory process, which is beginning to be associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 [22, 25].


5. Tronson NC, Taylor JR. Molecular mechanisms of memory reconsolidation. Nat Rev Neurosci. 2007; 8:262–275. [PubMed: 17342174]

6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

19. Tronel S, et al. Linking new information to a reactivated memory requires consolidation and not reconsolidation mechanisms. PLoS Biol. 2005; 3:e293. [PubMed: 16104829]

20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

21. Debiec J, LeDoux JE. Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala. Neuroscience. 2004; 129:267–272. [PubMed: 15501585]

22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

23. Taubenfeld SM, et al. The consolidation of new but not reactivated memory requires hippocampal C/EBP beta. Nat Neurosci. 2001; 4:813–818. [PubMed: 11477427]

24. Milekic MH, et al. Temporal requirement of C/EBPbeta in the amygdala following reactivation but not acquisition of inhibitory avoidance. Learn Mem. 2007; 14:504–511. [PubMed: 17644752]

25. Lee JLC, et al. Disrupting reconsolidation of drug memories reduces cocaine seeking behavior. Neuron. 2005; 47:795–801. [PubMed: 16157275]

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[As such, reconsolidation is a neurobiologically distinct memory process, which is] increasingly associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 (Lee et al., 2004, 2005).

The existence of reconsolidation processing is for the mostpart revealed by its absence. Quintessentially, when amnesia for a memory that is one or more days old is induced in a manner that is dependent upon the reactivation of said memory trace through retrieval, reconsolidation is considered to have been impaired (Nader et al., 2000; Dudai, 2004). However, similar to other cognitive functions, experimental treatments specifically aimed at targeting memory reconsolidation can also yield subsequent improvements (Tronson et al., 2006; Lee et al., 2006; Frenkel et al., 2005; Rodriguez et al., 1999; Blaiss & Janak, 2006). Further, the possibility to improve a memory trace through post-retrieval processing infers a potentially adaptive function for the reconsolidation process. Thus, instead of merely being process that restabilizes a memory following its retrieval, reconsolidation also represents a special state which allows for renewed memory plasticity and modulation (Dudai, 2007). Importantly, such memory-enhancing interventions include naturalistic phenomena such as water deprivation and the administration of glucose (Frenkel et al., 2005; Blaiss & Janak, 2006). Therefore, the ability to modify (e.g., strengthen) a previously acquired memory in a potentially adaptive manner is not limited to exogenous pharmacological treatment but is likely to be relevant to naturalistic situations of memory updating.

However, even in paradigms with well-established demonstrations of reactivation-dependent amnesia, there are conditions under which reconsolidation does not take place. Therefore, there exist certain boundary conditions around which reconsolidation may or may not be observed. First, temporal dynamics play an important role. In inhibitory avoidance in rats (Milekic & Alberini, 2002), as well as in fear conditioning in the medaka fish (Eisenberg & Dudai, 2004), 14-day-old memories did not demonstrate reactivation-dependent amnesia, [whereas younger memories did show evidence of reconsolidating.]

[page 3]

Therefore, reconsolidation is a neurobiologically-distinct memory process, which is beginning to be associated with specific cellular mechanisms, such as the expression of the immediate-early gene zif268 [22, 25].

The existence of a reconsolidation process is largely revealed by its absence. Typically, when amnesia for a memory that is one or more days old is induced in a manner that is dependent upon reactivation of that memory through retrieval, reconsolidation is said to have been impaired [4, 17]. However, in common with other cognitive functions, experimental treatments targeting memory reconsolidation can also result in subsequent improvements [26-30]. Gain-of-function findings are of particular importance in refuting non-specific accounts of amnesia. Moreover, the ability to improve a memory through postretrieval processing suggests a potentially adaptive function for the reconsolidation process. Rather than simply being process that restabilises a memory following its retrieval, it represents a special state, providing an opportunity for renewed memory plasticity and modulation [11]. Notably, the aforementioned memory-enhancing interventions include naturalistic phenomena such as water deprivation and the administration of glucose [28, 29]. Therefore, the capacity to modify (e.g. strengthen) a previously-acquired memory in a potentially adaptive manner is not limited to exogenous pharmacological treatment, but is likely also to be relevant to naturalistic situations of memory updating.

[page 5]

Even in paradigms with well-established demonstrations of reactivation-dependent amnesia, there are conditions under which reconsolidation does not take place. Therefore, there exist certain boundary conditions, which for the purposes of this review, are considered simply to be a description of the boundaries around which reconsolidation may or may not be observed. [...]

Other than the impact of memory strength, several boundary conditions exist. The first among these is temporal in nature. In inhibitory avoidance in rats [47], as well as in fear conditioning in the medaka fish [48], 14-day old memories did not display reactivationdependent amnesia, whereas younger memories did show evidence of reconsolidating.


4. Nader K, et al. Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature. 2000; 406:722–726. [PubMed: 10963596]

11. Dudai, Y. Post-activation state: a critical rite of passage of memories. In: Bontempi, B., et al., editors. Memories: Molecules and Circuits. Springer-Verlag; 2007. p. 69-82.

17. Dudai Y. The neurobiology of consolidations, or, how stable is the engram? Annu Rev Psychol. 2004; 55:51–86. [PubMed: 14744210]

22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

25. Lee JLC, et al. Disrupting reconsolidation of drug memories reduces cocaine seeking behavior. Neuron. 2005; 47:795–801. [PubMed: 16157275]

26. Tronson NC, et al. Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase A. Nat Neurosci. 2006; 9:167–169. [PubMed: 16415868]

27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

28. Frenkel L, et al. Memory strengthening by a real-life episode during reconsolidation: an outcome of water deprivation via brain angiotensin II. Eur J Neurosci. 2005; 22:1757–1766. [PubMed: 16197516]

29. Rodriguez WA, et al. Effects of glucose and fructose on recently reactivated and recently acquired memories. Prog Neuropsychopharmacol Biol Psychiatry. 1999; 23:1285–1317. [PubMed: 10581649]

30. Blaiss CA, Janak PH. Post-training and post-reactivation administration of amphetamine enhances morphine conditioned place preference. Behav Brain Res. 2006

47. Milekic MH, Alberini CM. Temporally Graded Requirement for Protein Synthesis following Memory Reactivation. Neuron. 2002; 36:521–525. [PubMed: 12408853]

48. Eisenberg M, Dudai Y. Reconsolidation of fresh, remote, and extinguished fear memory in medaka: old fears don’t die. Eur J Neurosci. 2004; 20:3397–3403. [PubMed: 15610172]

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However, this is not a universal finding, with contextual fear and appetitive cocaine-related memories showing reconsolidation up to a month following learning (Lee et al., 2006; Debiec et al., 2002). Nevertheless, it remains possible that all memories possess an age-dependent sensitivity to reconsolidation induced impairment, but with divergent time-courses thus far unaccounted for by the current literature. Alternatively, as suggested by Lee (2009), given that there is an interaction between memory age and the duration of stimulus re-exposure required to successfully reactivate a contextual fear memory (Suzuki et al., 2004), it is further possible that all memories undergo reconsolidation regardless of their age, but that previous studies have failed to employ sufficiently strong memory reactivation cues for older memories. However, as further purported by Lee, if the age of a memory does indeed represent a limit on the engagement of reconsolidation mechanisms, this might speculatively fit in with an updating hypothesis. Perhaps the passage of time, under certain circumstances, results in new experiences being more likely to be encoded separately from the original memory. As such it would be predicted that updating an old memory should engage consolidation specific mechanisms [e.g., brain-derived neurotrophic factor [BDNF] in the hippocampus for contextual fear memories (Lee et al., 2004)]. Moreover, selective interference with these mechanisms should only affect the new updating information, thereby resulting not in amnesia, as would be expected if reconsolidation mechanisms were being engaged and disrupted, but in a failure to modify the memory.

The issue concerning whether a new experience updates an existing memory trace or triggers new memory trace formation might also underlie the already established constraint that extinction places on reconsolidation. Memory reactivation protocols typically involve short extinction sessions. However, lengthier non-reinforced stimulus exposure reverses the impact of amnestic treatment.

However, this is by no means a universal finding, with contextual fear and appetitive cocaine-related memories reconsolidating up to a month after learning [42, 49]. Nevertheless, it remains possible that all memories do display an age-dependent sensitivity to reconsolidation impairment, but with different timecourses not yet revealed by the current literature. Alternatively, given that there is an interaction between memory age and duration of stimulus re-exposure required successfully to reactivate a contextual fear memory [50], it is also possible that all memories undergo reconsolidation regardless of their age, but that previous studies have failed to use sufficiently intense memory reactivation conditions for older memories. However, if the age of a memory does indeed represent a limit on the engagement of reconsolidation mechanisms, this might speculatively fit in with an updating hypothesis. Perhaps the passage of time, under certain circumstances, results in new experiences being more likely to be encoded separately from the original memory. A prediction of this view would be that updating an old memory should engage consolidation-specific mechanisms (e.g. BDNF in the hippocampus for contextual fear memories [22]). Moreover, selective interference with these mechanisms should affect only the new updating information, thus resulting not in amnesia, as would be expected if reconsolidation mechanisms were being engaged and disrupted, but in a failure to modify the memory.

The issue of whether a new experience updates an existing memory or triggers new memory formation may also underlie the established constraint that extinction places on reconsolidation. Memory reactivation protocols typically involve short extinction sessions. However, lengthier non-reinforced stimulus exposure reverses the impact of amnestic treatment.


22. Lee JLC, et al. Independent cellular processes for hippocampal memory consolidation and reconsolidation. Science. 2004; 304:839–843. [PubMed: 15073322]

42. Lee JLC, et al. Cue-induced cocaine seeking and relapse are reduced by disruption of drug memory reconsolidation. J Neurosci. 2006; 26:5881–5887. [PubMed: 16738229]

49. Debiec J, et al. Cellular and systems reconsolidation in the hippocampus. Neuron. 2002; 36:527– 538. [PubMed: 12408854]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

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[Therefore, in terms of contextual fear memories, protein] synthesis impairs reconsolidation in order to decrease fear when the context re-exposure is short, but conversely disrupts extinction in order to maintain high levels of fear when the duration of context re-exposure is more prolonged (Suzuki et al., 2004). Such a hypothesis has been replicated in cued fear memories (Lee et al., 2006) as well as in contextual aversive learning in the crab Chasmagnathus (Pedreira & Maldonado, 2003), although it appears that extinction does not always block reconsolidation from taking place (Duvarci et al., 2006). Thus, it is not merely the level of extinction training, but its relationship with initial learning that determines the interaction between reconsolidation and extinction. Protein synthesis inhibition during the same reactivation/extinction parameters has yielded opposing effects when the strength of initial training on a conditioned taste aversion task is varied (Eisenberg et al., 2003), which was conceptualised as a trace dominance process, whereby the dominant trace engaged by reactivation/extinction is that which is impacted upon by experimental treatment. However, instead of competition between traces, the extent of extinction training relative to conditioning may determine whether or not a new inhibitory memory is formed. Thus, if stimulus exposure is sufficient to engage extinction learning, this would not concomitantly modify the original excitatory memory. Alternatively, more limited exposure, would serve to trigger memory updating in the absence of new inhibitory learning. Providing support for such a contention is the recent finding in the crab that the transcription factor nuclear factor-kB (NF-kB) reflects a molecular switch between reconsolidation and extinction (Merlo & Romano, 2008). Inhibiting NFkB both impairs reconsolidation (Merlo et al., 2005) and enhances extinction (Merlo & Romano, 2008) under the appropriate conditions. Consequently, short memory reactivation induces a functional upregulation of NF-kB, whereas more prolonged extinction results in a functional inhibition. If the assumption is made that NF-kB activity is reflective of a reconsolidation/updating process, [the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.] [page 5]

Thus for contextual fear memories, protein synthesis impairs reconsolidation to reduce fear when the context re-exposure is short, but disrupts extinction to maintain high

[page 6]

levels of fear when the duration of context re-exposure is more prolonged [50]. This pattern of result has been replicated in cued fear memories [27] as well as in contextual aversive learning in the crab Chasmagnathus [51], though it appears that extinction does not always prevent reconsolidation from taking place [52]. It is not simply the level of extinction training, but its relation to initial learning, that governs the interaction between reconsolidation and extinction. Protein synthesis inhibition during the same reactivation/extinction parameters produced opposing effects when the strength of initial training on a conditioned taste aversion task was varied [53]. This has previously been conceptualised as a trace dominance process, whereby the dominant trace engaged by reactivation/extinction is that which is impacted upon by experimental treatment [53]. However, rather than appealing to competition between traces, the extent of extinction training relative to conditioning may determine whether or not a new inhibitory memory is formed. This argument states that if stimulus exposure is sufficient to engage extinction learning, this would not concomitantly modify the original excitatory memory. More limited exposure, by contrast, would trigger memory updating in the absence of new inhibitory learning. Perhaps in support of this interpretation is the recent finding in Chasmagnathus that the transcription factor NF-κB reflects a molecular switch between reconsolidation and extinction [54]. Inhibiting NF-κB both impairs reconsolidation [55] and enhances extinction [54] under the appropriate conditions. Consequently, short memory reactivation induces a functional upregulation of NF-κB, whereas more prolonged extinction results in a functional inhibition. If we make the assumption that NF-κB activity is reflective of a reconsolidation/updating process, the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.


27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

51. Pedreira ME, Maldonado H. Protein synthesis subserves reconsolidation or extinction depending on reminder duration. Neuron. 2003; 38:863–869. [PubMed: 12818173]

52. Duvarci S, et al. Extinction is not a sufficient condition to prevent fear memories from undergoing reconsolidation in the basolateral amygdala. Eur J Neurosci. 2006; 24:249–260. [PubMed: 16882021]

53. Eisenberg M, et al. Stability of retrieved memory: Inverse correlation with trace dominance. Science. 2003; 301:1102–1104. [PubMed: 12934010]

54. Merlo E, Romano A. Memory extinction entails the inhibition of the transcription factor NFkappaB. PLoS ONE. 2008; 3:e3687. [PubMed: 18997870]

55. Merlo E, et al. Activation of the transcription factor NF-kappaB by retrieval is required for longterm memory reconsolidation. Learn Mem. 2005; 12:23–29. [PubMed: 15687229]

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[If the assumption is made that NF-kB activity is reflective of a reconsolidation/updating process,] the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.

A further boundary condition on memory reconsolidation has recently been termed the ‘predictability of the reactivation stimulus’ (Nader & Hardt, 2009). This condition reflects findings emerging primarily from the crab literature that a mismatch between expected and actual events during reactivation triggers reconsolidation. Pedreira and colleagues (2004) found that reconsolidation only took place, and thus could only be disrupted, when the predictive context ended in the unexpected absence of the aversive outcome. It is not merely the case that memory reactivation must differ in some respect to conditioning, as there are numerous instances whereby reconsolidation impairments have been observed when the reactivation session is operationally identical to training (e.g., using reinforced reactivation procedures in fear conditioning (Eisenberg & Dudai, 2004; Duvarci & Nader, 2004), and in many (Kelly et al., 2003; Akirav & Maroun, 2006), but not all (Rossato et al., 2007) studies of object recognition memories). Instead, reconsolidation is triggered by a violation of expectation based upon prior learning, whether such a violation is qualitative (i.e., the outcome not occurring at all) or quantitative (i.e., the magnitude of the outcome not being fully predicted). It has thus been predicted that further initial training of fear or object memories would render such memories resistant to reconsolidation impairments through the use of reactivation sessions that are identical to training. Such an interpretation suggests that incompletely, but not fully, learned memories are subject to reconsolidation given the requirement for memory updating to optimize further the predictive accuracy of the memory.

Several hypotheses have been put forth regarding the role of reconsolidation in terms of wider memory processes. Two of these (Alberini, 2005; Dudai & Eisenberg, 2004) have adopted the temporal boundary condition to argue that reconsolidation plays a role in an extended process of memory stabilization.

[page 6]

If we make the assumption that NF-κB activity is reflective of a reconsolidation/updating process, the extinction-induced inhibition would be consistent with a suppression of memory updating in favour of new extinction learning.

A further boundary condition on memory reconsolidation has recently been termed the “predictability of the reactivation stimulus” [10]. This reflects the findings emerging primarily from the Chasmagnathus literature that a mismatch between expected and actual events during reactivation triggers reconsolidation. Pedreira et al. [56] found that reconsolidation only took place, and thus could only be disrupted, when the predictive context terminated in the unexpected absence of the aversive outcome. It is not simply that memory reactivation must differ in some manner to conditioning, as there are numerous instances where reconsolidation impairments have been observed when the reactivation session is operationally identical to training (e.g. using reinforced reactivation procedures in fear conditioning [48, 57], and in many [35, 58], but not all [59] studies of object recognition memories). Instead, reconsolidation is triggered by a violation of expectation based upon prior learning, whether such a violation is qualitative (the outcome not occurring at all) or quantitative (the magnitude of the outcome not being fully predicted). It is predicted, then, that more extended initial training of fear or object memories will render those memories resistant to reconsolidation impairments with the use of reactivation sessions that are identical to training. This interpretation, therefore, partially reduces to the prior discussion of memory strength, in that incompletely, but not fully, learned memories are subject to reconsolidation because of the requirement for memory updating in order to optimise further the predictive accuracy of the memory.

[page 7]

Several positions have been advanced regarding the role of reconsolidation in wider memory processes. Two of these [6, 8] have used the apparent temporal boundary condition to argue that reconsolidation plays a part in an extended process of memory stabilisation.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

10. Nader K, Hardt O. A Single Standard For Memory: The Case For Reconsolidation. Nature Reviews Neuroscience. 2009; 10:224–234.

35. Kelly A, et al. Activation of mitogen-activated protein kinase/extracellular signal-regulated kinase in hippocampal circuitry is required for consolidation and reconsolidation of recognition memory. J Neurosci. 2003; 23:5354–5360. [PubMed: 12832561]

48. Eisenberg M, Dudai Y. Reconsolidation of fresh, remote, and extinguished fear memory in medaka: old fears don’t die. Eur J Neurosci. 2004; 20:3397–3403. [PubMed: 15610172]

56. Pedreira ME, et al. Mismatch between what is expected and what actually occurs triggers memory reconsolidation or extinction. Learn Mem. 2004; 11:579–585. [PubMed: 15466312]

57. Duvarci S, Nader K. Characterization of fear memory reconsolidation. J Neurosci. 2004; 24:9269– 9275. [PubMed: 15496662]

58. Akirav I, Maroun M. Ventromedial prefrontal cortex is obligatory for consolidation and reconsolidation of object recognition memory. Cereb Cortex. 2006; 16:1759–1765. [PubMed: 16421330]

59. Rossato JI, et al. On the role of hippocampal protein synthesis in the consolidation and reconsolidation of object recognition memory. Learn Mem. 2007; 14:36–46. [PubMed: 17272651]

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[Specifically, Alberini (2005) suggests that] repeated reactivations (which might be implicit during sleep) gradually increase memory stability as part of a lengthy consolidation process, such that when sufficient time has elapsed a memory can no longer be disrupted, but it can be added to or modified. Dudai and Eisenberg (2004) similarly integrate reconsolidation within a ‘lingering consolidation’ process, whereby the reactivation and reconsolidation cycle progressively stabilizes a memory. In contrast to such emphases on reconsolidation enhancing memory stability, memory updating does not require that reconsolidation has an endogenous role to play in the ongoing processing of a memory trace that requires no further modification. Indeed, the reverse has been suggested (see Lee, 2009), in that a memory will persist in a stable and fixed form only if reconsolidation is not engaged, given that reconsolidation is the mechanistic instantiation of memory updating. Thus, reconsolidation only plays a role in enhancing memory stability if such enhancement is dependent upon modification of the memory. Instead of focusing on reconsolidation constraints, Morris and colleagues (2006) argue instead for a mode-based explanation of reconsolidation according to which the dual activation of retrieval and encoding states drives reconsolidation processes. This model is well suited to account for situations wherein new experiences result in profound changes to the memory; a change in the location of an escape platform in a water maze being the example used for the delayed non-mapping to place task. However, it is not clear either how it might be adapted to conditions of more negligible memory modifications (e.g., strength), or whether the activation of an ‘encoding mode’ is sufficient to trigger reconsolidation. For example, extinction training involves both memory retrieval as well as new memory encoding, but under such circumstances reconsolidation is not obviously engaged (e.g., Lee et al., 2006; Suzuki et al., 2004; Pedreira & Moldonado, 2003). Moreover, the mode requirement appears to be an additional, as opposed to an alternative, boundary condition to those already discussed. Specifically, Alberini [6] suggests that repeated reactivations (which may be implicit during sleep) gradually increase memory stability as part of a lengthy consolidation process, such that when sufficient time has elapsed, a memory can no longer be disrupted, but can be added to or modified. Dudai & Eisenberg [8] similarly integrate reconsolidation within a “lingering consolidation” process, whereby the reactivation and reconsolidation cycle progressively stabilises a memory (Fig. 1A). In contrast to these emphases on reconsolidation enhancing memory stability, the present focus on memory updating does not require that reconsolidation has an endogenous part to play in the ongoing processing of a memory that requires no further modification. Indeed, the reverse may be suggested, in that a memory will persist in a stable and fixed form only if reconsolidation is not engaged, precisely because reconsolidation is the mechanistic instantiation of memory updating. Thus reconsolidation only plays a part in enhancing memory stability if such enhancement is dependent upon modification of the memory.

Rather than focussing on parametric factors in the constraint of reconsolidation, Morris et al. [36] argue for a mode-based explanation. Namely it may be the dual activation of retrieval and encoding states that drives reconsolidation processes. This model is well suited to account for situations in which new experiences result in profound changes to the memory; a change in the location of an escape platform in a water maze being the example used for the delayed non-mapping to place task [36]. However, it is not clear either how it may be adapted to conditions of more minor memory modifications (such as strength), or whether the activation of an “encoding mode” is sufficient to trigger reconsolidation. For example, extinction training clearly involves memory retrieval as well as new memory encoding, but under such circumstances reconsolidation is not obviously engaged [27, 50, 51, 53]. Moreover, the mode requirement appears to be an additional, rather than alternative, boundary condition to those discussed previously.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

8. Dudai Y, Eisenberg M. Rites of passage of the engram: reconsolidation and the lingering consolidation hypothesis. Neuron. 2004; 44:93–100. [PubMed: 15450162]

27. Lee JLC, et al. Reconsolidation and extinction of conditioned fear: inhibition and potentiation. J Neurosci. 2006; 26:10051–10056. [PubMed: 17005868]

37. Rossato JI, et al. Retrieval induces hippocampal-dependent reconsolidation of spatial memory. Learn Mem. 2006; 13:431–440. [PubMed: 16882860]

50. Suzuki A, et al. Memory reconsolidation and extinction have distinct temporal and biochemical signatures. J Neurosci. 2004; 24:4787–4795. [PubMed: 15152039]

51. Pedreira ME, Maldonado H. Protein synthesis subserves reconsolidation or extinction depending on reminder duration. Neuron. 2003; 38:863–869. [PubMed: 12818173]

53. Eisenberg M, et al. Stability of retrieved memory: Inverse correlation with trace dominance. Science. 2003; 301:1102–1104. [PubMed: 12934010]

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[Alternately, a hypothesis based upon memory updating incorporates] both the principles of the dual state hypothesis (in that a requirement for updating depends upon the same conditions as those proposed to engage an encoding state), and can potentially account for other boundary conditions.

Further, Ortiz and Bermudez-Rattoni (2007) postulate reconsolidation as an ‘updating consolidation’ mechanism. Further to demonstrating that fully learned memories are not subject to reactivation-dependent amnesia, these researchers found in both spatial and taste memories that when learning had reached near-asymptotic levels, only partial amnesia resulted from reactivation and protein synthesis inhibition (Rodriguez-Ortiz et al., 2005, 2008). This partial amnesia was considered to reflect only the partial destabilization of the existing memory trace to enable updating. As such, this idea is not dissimilar to Alberini’s previously discussed contention that old memories can be updated, but not disrupted (2005). Moreover, Rodriguez- Ortiz and Bermudez-Rattoni suggest that reconsolidation associated response decrements do not reflect memory loss for the original consolidated memory but, rather, emanate from a failure to integrate new learning, thereby leading to interference. However, such an interpretation cannot account for recent findings in terms of contextual fear memories (e.g., Lee, 2008). If reconsolidation impairments result from new learning interfering with the stable old memory trace, disruption of the new learning itself should result in an unchanged memory (Lee, 2009). However, in Lee’s (2008) recent study, this is not what was observed when the consolidation-specific protein BDNF was knocked down2 in the hippocampus during memory strengthening/updating. Instead, while knocking down BDNF had no impact on memory strengthening, the modification of the old memory was completely dependent upon the reconsolidation-selective upregulation of zif268.


[2 Gene knockdown refers to techniques by which the expression of one or more of an organism's genes is reduced, either through genetic modification (a change in the DNA of one of the organism's chromosomes) or by treatment with a reagent such as a short DNA or RNA oligonucleotide with a sequence complementary to either an mRNA transcript or a gene.]

A hypothesis based upon memory updating, in contrast, both incorporates the principles of the dual state proposal (in that a requirement for updating depends upon the same conditions as those proposed to engage an encoding state), and can potentially account for other boundary conditions.

Boundary conditions on memory reconsolidation also influence a further hypothesis of memory updating that is superficially similar to that advanced here. Rodriguez-Ortiz & Bermudez-Rattoni [60] conceive of reconsolidation as an “updating consolidation” mechanism (Fig. 1B). As well as showing that fully-learned memories are not subject to reactivation-dependent amnesia, these authors observed in both spatial and taste memories that when learning had reached near-asymptotic levels, only partial amnesia resulted from reactivation and protein synthesis inhibition [43, 44]. This partial amnesia is inferred to reflect only the partial destabilisation of the existing memory trace to enable updating. As such, this idea is not dissimilar to Alberini’s suggestion that old memories can be updated, but not disrupted [6]. Moreover, Rodriguez-Ortiz & Bermudez-Rattoni suggest that reconsolidation-associated response decrements do not reflect memory loss for the original consolidated memory, but rather result from a failure to integrate new learning, leading to interference. However, such an interpretation cannot account for my recent results in contextual fear memories [20]. If reconsolidation impairments result from new learning interfering with the stable old memory trace, disruption of the new learning itself should result in an unchanged memory. This is not what was observed when the consolidation-specific protein BDNF was knocked down in the hippocampus during memory strengthening/updating. Instead, while knocking down BDNF had no impact on memory strengthening, the modification of the old memory was completely dependent upon the reconsolidation-selective upregulation of zif268.


6. Alberini CM. Mechanisms of memory stabilization: are consolidation and reconsolidation similar or distinct processes? Trends Neurosci. 2005; 28:51–56. [PubMed: 15626497]

20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

43. Rodriguez-Ortiz CJ, et al. Protein synthesis underlies post-retrieval memory consolidation to a restricted degree only when updated information is obtained. Learn Mem. 2005; 12:533–537. [PubMed: 16166395]

44. Rodriguez-Ortiz CJ, et al. Intrahippocampal anisomycin infusions disrupt previously consolidated spatial memory only when memory is updated. Neurobiol Learn Mem. 2008; 89:352–359. [PubMed: 18054256]

60. Rodriguez-Ortiz, CJ.; Bermudez-Rattoni, F. Memory reconsolidation or updating consolidation?. In: Bermudez-Rattoni, F., editor. Neural plasticity and memory: From genes to brain imaging. Taylor and Francis Group; 2007. p. 209-224.

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[Also,] interference with memory destabilization both protected against the disruptive effects of protein synthesis inhibition and fixed the memory at the same strength despite additional learning. Thus, memory updating requires the destabilization of the original memory in order in integrate new information. Consequently, impairment of the restabilization process (e.g., through protein synthesis inhibition) affects not only the new information but also the reactivated memory, thereby leading to amnesia. Furthermore, interfering with memory

[page 8]

destabilisation both protected against the disruptive effects of protein synthesis inhibition and fixed the memory at the same strength in spite of further learning [20]. Therefore, memory updating requires the destabilisation of the original memory in order in integrate new information. As a result, impairment of the restabilisation process (e.g. through protein synthesis inhibition) affects not only the new information, but also the reactivated memory, thus leading to amnesia (Fig. 1C).


20. Lee JLC. Memory reconsolidation mediates the strengthening of memories by additional learning. Nat Neurosci. 2008; 11:1264–1266. [PubMed: 18849987]

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Providing succinct answers to such questions is integral given that the reconsolidation phase has been seized upon as crucial for the understanding of memory stability and, more recently, as a potential therapeutic target in the treatment of disorders such as post traumatic stress and drug addiction. Presently, little is known about the reactivation process, or what might be the adaptive function of retrieval-induced plasticity. Reconsolidation has long been proposed to mediate memory updating, but only recently has this hypothesis been supported experimentally. The reconsolidation phase has been seized upon as critical for the understanding of memory stability, and more recently as a potential therapeutic target in the treatment of disorders such as post-traumatic stress and drug addiction. However, little is known about the reactivation process, nor what might be the adaptive function of retrieval-induced plasticity. Reconsolidation has long been proposed to mediate memory updating, but only recently has this hypothesis been supported experimentally.
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