In:
revneuro, Walter de Gruyter GmbH, Vol. 22, No. 2 ( 2011-04-01), p. 205-229
Abstract:
Memories are fragile and easily forgotten at first, but after a consolidation period of hours to weeks, are inscribed in our brains as stable traces, no longer vulnerable to conventional amnesic treatments. Retrieval of a memory renders it labile, akin to the early stages of consolidation. This phenomenon has been explored as memory reactivation, in the sense that the memory is temporarily ‘deconsolidated’, allowing a short time window for amnesic intervention. This window closes again after reconsolidation, which restores the stability of the memory. In contrast to this ‘transient deconsolidation’ and the short-spanned amnesic effects of consolidation blockers, some specific treatments can disrupt even consolidated memory, leading to apparent amnesia. We propose the term ‘ amnesic deconsolidation ’ to describe such processes that lead to disruption of consolidated memory and/or consolidated memory traces. We review studies of these ‘amnesic deconsolidation’ treatments that enhance memory extinction, alleviate relapse, and reverse learning-induced plasticity. The transient deconsolidation that memory retrieval induces and the amnesic deconsolidation that these regimes induce both seem to dislodge a component that stabilizes consolidated memory. Characterizing this component, at both molecular and network levels, will provide a key to developing clinical treatments for memory-related disorders and to defining the consolidated memory trace.
Type of Medium:
Online Resource
ISSN:
2191-0200
,
0334-1763
DOI:
10.1515/rns.2011.023
Language:
English
Publisher:
Walter de Gruyter GmbH
Publication Date:
2011
detail.hit.zdb_id:
2598365-9
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