When reactivated, memories enter a labile, protein synthesis–dependent state, a process referred to as reconsolidation. Here, we show in rats that fear memory retrieval produces a synaptic potentiation in the lateral amygdala that is selective to the reactivated memory, and that disruption of reconsolidation is correlated with a reduction of synaptic potentiation in the lateral amygdala. Thus, both retrieval and reconsolidation alter memories via synaptic plasticity at selectively targeted synapses.
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This research was supported by grants to J.E.L. (Public Health Service, National Institutes of Health Grants R37 MH38774, R01 MH46516, P50 MH58911 and K05 MH067048, Volkswagen-Stiftung Grant I- 79 894 and Human Frontier Science Program Grant RGP0094-2001-B). M.-H.M is funded by the Alberta Heritage Foundation for Medical Research and the Natural Science and Engineering Research Council. V.D. is funded by EU FP6 frameprogram-integrated project PROMEMORIA, Centre National de la Recherche Scientifique–National Science Foundation Grant 17089 and CNRS-PICS.
The authors declare no competing financial interests.
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Doyère, V., Dębiec, J., Monfils, MH. et al. Synapse-specific reconsolidation of distinct fear memories in the lateral amygdala. Nat Neurosci 10, 414–416 (2007). https://doi.org/10.1038/nn1871
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