Cited by 184Memory and Neural MechanismsStress Responses and CortisolNeuroscience and Neuropharmacology Research

Amygdalar Inactivation Blocks Stress-Induced Impairments in Hippocampal Long-Term Potentiation and Spatial Memory

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Kim, Jeansok J., Koo, Ja Wook, Lee, Hongjoo J., Han, Jung-Soo·2005·The Journal of Neuroscience

Abstract

Electrolytic lesions to the amygdala, a limbic structure implicated in stress-related behaviors and memory modulation, have been shown to prevent stress-induced impairments of hippocampal long-term potentiation (LTP) and spatial memory in rats. The present study investigated the role of intrinsic amygdalar neurons in mediating stress effects on the hippocampus by microinfusing the GABA(A) receptor agonist muscimol into the amygdala and examining stress effects on Schaffer collateral/commissural-CA1 LTP and spatial memory. The critical period of the amygdalar contribution to stress effects on hippocampal functions was determined by applying muscimol either before stress or immediately after stress. Our results indicate that intra-amygdalar muscimol infusions before uncontrollable restraint-tailshock stress effectively blocked stress-induced physiological and behavioral effects. Specifically, hippocampal slices prepared from vehicle-infused stressed animals exhibited markedly impaired LTP, whereas slices obtained from muscimol-infused stressed animals demonstrated robust LTP comparable with that of unstressed animals. Correspondingly, vehicle-infused stressed animals displayed impaired spatial memory (on a hidden platform version of the Morris water maze task), whereas muscimol-infused stressed animals revealed unimpaired spatial memory. In contrast to prestress muscimol effects, however, immediate poststress infusions of muscimol into the amygdala failed to interfere with stress impairments of LTP and spatial memory. Together, these results suggest that the amygdalar neuronal activity during stress, but not shortly after stress, is essential for the emergence of stress-induced alterations in hippocampal LTP and memory.

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Crossref · 10.1523/jneurosci.4623-04.2005

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Authors
Kim, J. J., Koo, J. W., Lee, H. J., & Han, J.-S.
Affiliations
  • University of Washington (US)
  • Yale University (US)
  • Johns Hopkins University (US)
Venue
The Journal of Neuroscience
Published
2005-02-09
Volume
25
Issue
6
Pages
1532-1539
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W2053502537
Cited by
184
References
71
Citations by year
2026: 2 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 8 · 2020: 3 · 2019: 4 · 2018: 6 · 2017: 6 · 2016: 12 · 2015: 6 · 2014: 14 · 2013: 19 · 2012: 16
FWCI
7.12
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Whitehall Foundation
  • National Institute of Mental Health (MH64457, R01MH064457, 1R01 MH64457)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
amygdala, stress, hippocampal long-term potentiation, spatial memory, muscimol, GABAA receptor, stress-induced memory impairment, limbic system
MeSH terms
Amygdala, Animals, Corticosterone, Drug Administration Schedule, Electroshock, Hippocampus, Male, Memory Disorders, Muscimol, Stress, Physiological, Vocalization, Animal, Rats, Sprague-Dawley, Long-Term Potentiation, GABA Agonists, Maze Learning, Rats, GABA-A Receptor Agonists

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