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| Untersuchte Arbeit: Seite: 48, Zeilen: 1-25 |
Quelle: Lee 2009 Seite(n): 5, 6, Zeilen: 5: last lines - 6: 1-23 |
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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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