Nature Neuroscience 9, 167 - 169 (2006)
Published online: 15 January 2006; Corrected online: 02 May 2006 | doi:10.1038/nn1628
Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase ANatalie C Tronson1, 2, Shari L Wiseman1, Peter Olausson1
& Jane R Taylor1, 21
Department of Psychiatry, Division of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine, Abraham Ribicoff Research Facilities, Connecticut Mental Health Center, 34 Park Street, New Haven, Connecticut 06508, USA. 2
Department of Psychology, Yale University, 2 Hillhouse Avenue, New Haven, Connecticut 06520, USA.
Correspondence should be addressed to Jane R Taylor jane.taylor@yale.edu 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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