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The Journal of Neuroscience, April 1, 2001, 21(7):2518-2525
Basolateral Amygdala-Nucleus Accumbens Interactions in Mediating
Glucocorticoid Enhancement of Memory Consolidation
Benno
Roozendaal,
Dominique J.-F.
de Quervain,
Barbara
Ferry,
Barry
Setlow, and
James L.
McGaugh
Center for the Neurobiology of Learning and Memory and Department
of Neurobiology and Behavior, University of California, Irvine,
California 92697-3800
Systemic or intracerebral administration of glucocorticoids
enhances memory consolidation in several tasks. Previously, we reported
that these effects depend on an intact basolateral nucleus of the
amygdala (BLA) and efferents from the BLA that run through the stria
terminalis (ST). The BLA projects directly to the nucleus accumbens
(NAc) via this ST pathway. The NAc also receives direct projections
from the hippocampus and, therefore, may be a site of convergence of
BLA and hippocampal influences in modulating memory consolidation. In
support of this view, we found previously that lesions of either the
NAc or the ST also block the memory-modulatory effect of systemically
administered glucocorticoids. The present experiments examined the
effects of lesions of the NAc or the ST on the memory-modulatory
effects of intracerebral glucocorticoids on inhibitory
avoidance training. Microinfusions of the
specific glucocorticoid receptor agonist
11 ,17-dihydroxy-6,21-dimethyl-17 -pregna-4,6-trien-20yn-3-one (RU 28362; 1.0 or 3.0 ng) into either the BLA or the hippocampus of
male Sprague Dawley rats administered immediately after training enhanced the 48 hr retention performance in a dose-dependent manner. Bilateral lesions of the NAc or the ST alone did not affect retention performance but blocked the memory enhancement induced by intra-BLA or
intrahippocampal glucocorticoid receptor agonist administration. These
findings indicate that the BLA-NAc pathway plays an essential role in
mediating glucocorticoid effects on memory consolidation and suggest
that the BLA interacts with hippocampal effects on memory consolidation
via this pathway.
Key words:
hippocampus; inhibitory avoidance; memory storage; stria
terminalis; RU 28362; ventral striatum
Copyright © 2001 Society for Neuroscience 0270-6474/01/2172518-08$05.00/0
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