Abstract
Reconsolidation—the stabilization of a memory after retrieval—is hypothesized to be a critical and distinct component of memory processing, the disruption of which results in memory impairment. In the rat, we found that activation of amygdalar protein kinase A (PKA) was sufficient to enhance memory only when it was retrieved; in contrast, PKA inhibition impaired reconsolidation. This study demonstrates both a selective enhancement and an impairment of memory reconsolidation dependent on amygdalar PKA.
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Change history
02 May 2006
Replaced Supplementary Methods file
Notes
NOTE: In the version of this article intially published online, the units for some of the values in the Supplementary Methods incorrectly said L. The correct unit should be µM. This error has been corrected.
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Acknowledgements
We thank J.J. Quinn for her comments on the manuscript. This work was supported by grant DA15222 from the US National Institute on Drug Abuse and grant MH25642 from the National Institute of Mental Health. N.C.T. was supported in part by a Robert F. Leylan Yale University Fellowship.
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Supplementary information
Supplementary Fig. 1
Schematic representation of injector placements in basolateral amygdala (BLA). (PDF 934 kb)
Supplementary Fig. 2
PKA activation in the basolateral amygdala does not affect freezing to the reactivation context. (PDF 195 kb)
Supplementary Fig. 3
Inhibition of PKA in the basolateral amygdala does not affect freezing to the reactivation context. (PDF 123 kb)
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Tronson, N., Wiseman, S., Olausson, P. et al. Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase A. Nat Neurosci 9, 167–169 (2006). https://doi.org/10.1038/nn1628
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DOI: https://doi.org/10.1038/nn1628
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