Behavioral stress modifies hippocampal plasticity through N-methyl-D-aspartate receptor activation.
Open accessAbstract
Behavioral stress has detrimental effects on subsequent cognitive performance in many species, including humans. For example, humans exposed to stressful situations typically exhibit marked deficits in various learning and memory tasks. However, the underlying neural mechanisms by which stress exerts its effects on learning and memory are unknown. We now report that in adult male rats, stress (i.e., restraint plus tailshock) impairs long-term potentiation (LTP) but enhances long-term depression (LTD) in the CA1 area of the hippocampus, a structure implicated in learning and memory processes. These effects on LTP and LTD are prevented when the animals were given CGP39551 (the carboxyethylester of CGP 37849; DL-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, before experiencing stress. In contrast, the anxiolytic drug diazepam did not block the stress effects on hippocampal plasticity. Thus, the effects of stress on subsequent LTP and LTD appear to be mediated through the activation of the NMDA subtype of glutamate receptors. Such modifications in hippocampal plasticity may contribute to learning and memory impairments associated with stress.
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NMDA receptor blockade during stress blocks the stress-induced suppression of LTP.
“Support for this hypothesis is the finding that NMDA receptor blockade during stress blocks the stress-induced suppression of LTP (Kim et al. [121]).”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Kim et al. [121]
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- Authors
- Kim, J. J., Foy, M. R., & Thompson, R. F.
- Affiliations
- University of Southern California (US)
- ORCID
- Kim, J J
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1996-05-14
- Volume
- 93
- Issue
- 10
- Pages
- 4750-4753
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC39350
- OpenAlex
- W2088939071
- Cited by
- 435
- References
- 2
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 6 · 2020: 11 · 2019: 8 · 2018: 11 · 2017: 11 · 2016: 9 · 2015: 18 · 2014: 22 · 2013: 13 · 2012: 33
- FWCI
- 4.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (8718300)
- Loyola Marymount University
- National Institutes of Health (AG05142)
- National Institute on Aging (AG 05142, P50AG005142)
- National Institute of Mental Health
- National Institute of Nursing Research (1F32MN10521-01BNR)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- behavioral stress, hippocampal plasticity, NMDA receptor, long-term potentiation, long-term depression, CA1, diazepam, learning and memory impairment, glutamate receptors
- MeSH terms
- Animals, Behavior, Animal, Hippocampus, Humans, Infant, Newborn, Learning, Male, Memory, Neuronal Plasticity, Stress, Physiological, 2-Amino-5-phosphonovalerate, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Excitatory Amino Acid Antagonists, Rats
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