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|Quelle: Lee 2009|
Seite(n): 3, 5, Zeilen: 3: 14-32; 5: 14-18, 22-25
|[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.]
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 . 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.
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 , as well as in fear conditioning in the medaka fish , 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]
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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]
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