Titre du document / Document title
Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval
Auteur(s) / Author(s)
NADER K. (1) ;
SCHAFE G. E. (1) ;
LE DOUX J. E. (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) W. M. Keck Foundation Laboratory of Neurobiology, Center for Neural Science, New York University, New York, New York 10003, ETATS-UNIS
Résumé / Abstract
'New' memories are initially labile and sensitive to disruption before being consolidated into stable long-term memories
1-5. Much evidence indicates that this consolidation involves the synthesis of new proteins in neurons
6-9. The lateral and basal nuclei of the amygdala (LBA) are believed to be a site of memory storage in fear learning
10. Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents consolidation of fear memories. Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning. The same treatment with anisomycin, in the absence of memory reactivation, left memory intact. Consistent with a time-limited role for protein synthesis production in consolidation, delay of the infusion until six hours after memory reactivation produced no amnesia. Our data show that consolidated fear memories, when reactivated, return to a labile state that requires de novo protein synthesis for reconsolidation. These findings are not predicted by traditional theories of memory consolidation.
Revue / Journal Title
Nature
ISSN
0028-0836
CODEN NATUAS
Source / Source
2000, vol. 406, n
o6797, pp. 722-726 (30 ref.)
Langue / Language
Anglais
Editeur / Publisher
Nature Publishing Group, London, ROYAUME-UNI
(1869)
(Revue)
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Localisation / Location
INIST-CNRS, Cote INIST : 142, 35400009116378.0220
Nº notice refdoc (ud4) : 1520927