von Dr. Jennifer L. Moore
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| [1.] Jm/Fragment 051 01 - Diskussion Zuletzt bearbeitet: 2014-02-19 00:24:52 Hindemith | BauernOpfer, Fragment, Gesichtet, Jm, Lee 2009, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 51, Zeilen: 1-22 |
Quelle: Lee 2009 Seite(n): 7, Zeilen: 28-51 |
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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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