Cited by 57Stress Responses and CortisolNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

Site and time dependent effects of acute stress on hippocampal long-term potentiation in freely behaving rats

Yamada, Kazuo, McEwen, Bruce S., Pavlides, Constantine·2003·Experimental Brain Research

Abstract

The phasic effects of stress-induced elevations of corticosterone on long-term potentiation (LTP) were investigated in the hippocampus of awake, freely behaving rats. Field potential recordings were performed in the dentate gyrus with stimulation of the medial perforant pathway or the CA1 with stimulation of the commissural/associational pathway, on the contralateral hemisphere. LTP was induced either shortly (1 h) after acute stress or 4 h later. Animals were either adrenalectomized or adrenally intact. A subgroup of animals were injected with a low dose of dexamethasone 4 h prior to the stressor, in order to suppress the corticosterone response to restraint stress, and they were tested for LTP in the dentate gyrus 4 h after the stressor. In the dentate gyrus, stress had no effect on LTP induction at 1 h post-stress; however, it produced a significant suppression at the 4 h interval. As expected, adrenalectomized rats did not show stress-suppression of LTP, but showed a lower level of LTP with or without stress. Supporting a role of stress-induced glucocorticoid secretion in LTP suppression, dexamethasone treatment of adrenally intact animals blocked the acute stress suppression of LTP in the dentate gyrus. In the CA1 field, restraint stress did not significantly affect LTP induction at either the 1- or 4-h post-stress intervals. Similarly, stress by itself, did not significantly affect neuronal excitability in either the dentate gyrus or CA1 hippocampal field at either the…

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Crossref · 10.1007/s00221-003-1519-0

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  • In many studies, acute, mild restraint stress had subtle or no effects on LTP, or if brief, could even enhance LTP.

    “In many studies, acute, mild restraint stress had subtle or no effects on LTP23, or if brief, could even enhance LTP29.”

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Authors
Yamada, K., McEwen, B. S., & Pavlides, C.
Affiliations
Rockefeller University (US)
Corresponding author
Pavlides, Constantine
Venue
Experimental Brain Research
Published
2003-09-01
Volume
152
Issue
1
Pages
52-59
ISSN
  • 0014-4819 (ISSN-L)
  • 1432-1106
OpenAlex
W2087084317
Cited by
57
References
4
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 4 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 4
FWCI
1.38
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Brain Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns035976-03)
  • National Institute of Neurological Disorders and Stroke (NS35976)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
acute stress, hippocampal long-term potentiation, corticosterone, glucocorticoids, dentate gyrus, CA1, restraint stress, adrenalectomy, dexamethasone, synaptic plasticity, hippocampal subfields, time-dependent effects, neuronal excitability
MeSH terms
Acute Disease, Adrenalectomy, Animals, Dexamethasone, Hippocampus, Male, Stress, Physiological, Time Factors, Wakefulness, Rats, Sprague-Dawley, Long-Term Potentiation, Excitatory Postsynaptic Potentials, Rats

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