Behavioral stress impairs long-term potentiation in rodent hippocampus
Abstract
A number of hormones secreted from the pituitary-adrenal system during stress affect learning and memory processes. The phenomenon of hippocampal long-term potentiation (LTP) is viewed by many as a putative mechanism of memory storage and has proved a most valuable model for study of neuronal plasticity at the cellular level. The present study was conducted to investigate the possibility that stressful events which occur prior (in vivo) to the preparation of brain slices may influence the electrophysiology of the in vitro hippocampal explant when tested for LTP. Adult male rats (Long-Evans male X Sprague-Dawley female) were pair-housed 1 week prior to testing. One animal in each pair was either placed in a restraining tube for 30 min and received no tail shocks (Restraint) or placed in a restraining tube and received tail shocks (1 microA, 1 s) every minute for 30 min (Restraint + Shock). The other animal in each pair was taken directly from the home cage and received no restraint or tail shock (Control). In vitro hippocampal slices were then prepared immediately from these animals according to standard methods. Our results demonstrate a marked impairment of LTP in hippocampal explants taken from rats exposed to stress. The significance of this result with respect to cellular mechanisms underlying the relationship between stress, cognition, and learning is discussed.
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Stress (restraint with or without tail shock) blocked the induction of LTP in CA1 in vitro.
“The first electrophysiological evidence that stress inhibited hippocampal functioning was provided by Richard Thompson and his coworkers, with their finding that stress (restraint with or without tail shock) blocked the induction of LTP in CA1 in vitro (Foy et al. [73]).”
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 Foy et al. [73]
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- Authors
- Foy, M. R., Stanton, M. E., Levine, S., & Thompson, R. F.
- Affiliations
- Stanford University (US)
- Corresponding author
- Foy, Michael R.
- ORCID
- Stanton, Mark E.
- Venue
- Behavioral and Neural Biology
- Publisher
- Elsevier BV
- Published
- 1987-07
- Volume
- 48
- Issue
- 1
- Pages
- 138-149
- ISSN
- 0163-1047 (ISSN-L)
- OpenAlex
- W2021113234
- Cited by
- 436
- References
- 3
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 1 · 2022: 6 · 2021: 4 · 2020: 10 · 2019: 14 · 2018: 13 · 2017: 8 · 2016: 4 · 2015: 12 · 2014: 17 · 2013: 14 · 2012: 21
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioral and Neural Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH-15147, MH-19936)
- 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
- long-term potentiation, hippocampus, stress, restraint stress, tail shock, pituitary-adrenal axis, hippocampal slices, neuroplasticity, memory, learning, stress hormones
- MeSH terms
- Animals, Cognition, Corticosterone, Electroshock, Female, Hippocampus, Learning, Male, Synaptic Transmission, Neuronal Plasticity, Rats, Inbred Strains, Restraint, Physical, Stress, Psychological, Synapses, Rats
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