Cited by 293Memory and Neural MechanismsStress Responses and CortisolMemory Processes and Influences

Basolateral amygdala noradrenergic influence enables enhancement of memory consolidation induced by hippocampal glucocorticoid receptor activation

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Roozendaal, Benno, Nguyen, Bichngoc T., Power, Ann E., McGaugh, James L.·1999·Proceedings of the National Academy of Sciences

Abstract

Previously, we reported that bilateral excitotoxic lesions of the basolateral nucleus of the amygdala (BLA) block the enhancing effects of posttraining systemic or intrahippocampal glucocorticoid administration on memory for inhibitory avoidance training. The present study further examined the basis of this permissive influence of the BLA on hippocampal memory functioning. Immediate posttraining unilateral infusions of the specific glucocorticoid receptor agonist RU 28362 (11β,17β-dihydroxy-6,21-dimethyl-17α-pregna-4,6-trien-20-yn-3-one; 3.0, 10.0, or 30.0 ng in 0.5 μl) administered into the dorsal hippocampus of male Sprague–Dawley rats induced dose-dependent enhancement of 48-h inhibitory avoidance retention. Infusions of the β-adrenoceptor antagonist atenolol (0.5 μg in 0.2 μl) into the ipsilateral, but not the contralateral, BLA 10 min prior to training blocked the hippocampal glucocorticoid effects on memory consolidation. Infusions of the muscarinic cholinergic antagonist atropine (0.5 μg in 0.2 μl) into either the ipsilateral or contralateral BLA before training did not block the hippocampal glucocorticoid effects. These findings provide further evidence that β-adrenergic activity in the BLA is essential in enabling glucocorticoid-induced modulation of memory consolidation and are consistent with the hypothesis that the BLA regulates the strength of memory consolidation in other brain structures. The ipsilateral nature of the BLA–hippocampus interaction indicates that BLA influences on hippocampal memory processes are mediated through neural pathways rather than by influences by means of the activation of peripheral stress responses.

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Crossref · 10.1073/pnas.96.20.11642

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Authors
Roozendaal, B., Nguyen, B. T., Power, A. E., & McGaugh, J. L.
Affiliations
University of California, Irvine (US)
Venue
Proceedings of the National Academy of Sciences
Published
1999-09-28
Volume
96
Issue
20
Pages
11642-11647
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1993475532
Cited by
293
References
4
Citations by year
2026: 5 · 2024: 1 · 2023: 3 · 2022: 5 · 2021: 10 · 2020: 5 · 2019: 4 · 2018: 22 · 2017: 14 · 2016: 11 · 2015: 10 · 2014: 8 · 2013: 7 · 2012: 11
FWCI
7.44
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of California, Irvine
  • National Institute of Mental Health (R01MH012526, MH12526, R56MH012526)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
Keywords
basolateral amygdala, hippocampus, memory consolidation, glucocorticoid receptor, RU 28362, beta-adrenergic activity, atenolol, noradrenergic modulation, passive avoidance, stress hormones, excitotoxic lesions
MeSH terms
Amygdala, Animals, Arousal, Atenolol, Dose-Response Relationship, Drug, Emotions, Hippocampus, Male, Memory, Norepinephrine, Receptors, Adrenergic, beta, Receptors, Glucocorticoid, Rats, Sprague-Dawley, Rats

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