Bidirectional behavioral plasticity of memory reconsolidation depends on amygdalar protein kinase A.
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.
Tronson
Natalie C
NC
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.
Wiseman
Shari L
SL
Olausson
Peter
P
Taylor
Jane R
JR
D000161:Acoustic Stimulation; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001522:Behavior, Animal / Q000502:physiology*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D005239:Fear / Q000502:physiology; D008568:Memory / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats
D017868:Cyclic AMP-Dependent Protein Kinases