TY - JOUR
T1 - Modulation of fear memory by retrieval and extinction
T2 - A clue for memory deconsolidation
AU - Hong, Ingie
AU - Kim, Jeongyeon
AU - Song, Beomjong
AU - Park, Sungmo
AU - Lee, Junuk
AU - Kim, Jihye
AU - An, Bobae
AU - Lee, Sukwon
AU - Choi, Sukwoo
N1 - Funding Information:
We thank the members of Gregory J. Quirk’s lab and Junchol Park for valuable discussion and comments on the work leading to this review. This work was supported by the Korea Institute of Science and Technology Grants (2E21510-10-004, 2E20970-09-058) and the Korea Science and Engineering Foundation Grant R01-2007-000-11323-0 (2007-0054261) funded by the Korean Ministry of Science and Technology. I.H., J.K., S.L., B.S., S.P., and J.K. were supported by the BK21 Research Fellowship from the Ministry of Education, Science and Technology, Republic of Korea.
PY - 2011/4/1
Y1 - 2011/4/1
N2 - 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.
AB - 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.
KW - amnesia
KW - deconsolidation
KW - extinction
KW - fear memory
KW - memory retrieval
KW - modulation
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U2 - 10.1515/RNS.2011.023
DO - 10.1515/RNS.2011.023
M3 - Article
C2 - 21476941
AN - SCOPUS:79954627129
VL - 22
SP - 205
EP - 229
JO - Reviews in the Neurosciences
JF - Reviews in the Neurosciences
SN - 0334-1763
IS - 2
ER -