Stress: metaplastic effects in the hippocampus
Open accessAbstract
Memory impairments, which occur regularly across species as a result of aging, disease and psychological insults (for example, stress), constitute a useful area for investigation into the neurobiological basis of learning and memory. Memory researchers have identified the hippocampus as a crucial brain structure involved in key aspects of memory formation. The most widely accepted putative mechanisms of memory storage in this structure are LTP and LTD. The hippocampus is enriched with receptors for corticosterone (a glucocorticoid hormone released in response to stress) and it plays a role in glucocorticoid negative feedback and, therefore, some hippocampal functioning might be particularly susceptible to stress. In support of this view, stress-induced modifications in learning, synaptic plasticity and endangerment of neurons have been seen in the hippocampus. Stress and glucocorticoids appear to exert a metaplastic effect through the modulation of Ca2+ levels. We propose a synaptic model that provides a conceptual scaffold to structure our understanding of the manifold actions of stress on the hippocampus. Accordingly, we suggest that stress-induced metaplasticity could disrupt Ca2+ homeostasis and thus endanger hippocampal neurons.
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More severe acute stressors impair hippocampal functions but continue to strengthen emotional associations and motor habits carried out by the amygdala and striatum.
“More severe acute stressors impair hippocampal functions38 but continue to strengthen the emotional associations and motor habits carried out by the amygdala and striatum, respectively14,39.”
From Stress signalling pathways that impair prefrontal cortex structure and function (2009) · cites this paper as [38]
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- Authors
- Kim, J. J., & Yoon, K. S.
- Affiliations
- Yale University (US)
- ORCID
- Kim, Jeansok J
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 1998-12
- Volume
- 21
- Issue
- 12
- Pages
- 505-509
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W1967552122
- Cited by
- 403
- References
- 5
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 10 · 2021: 14 · 2020: 8 · 2019: 12 · 2018: 16 · 2017: 12 · 2016: 10 · 2015: 9 · 2014: 20 · 2013: 14 · 2012: 14
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Trends in Neurosciences (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (5 T32 NS07224, T32NS007224)
- 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
- stress, hippocampus, metaplasticity, corticosterone, glucocorticoids, long-term potentiation, long-term depression, synaptic plasticity, calcium homeostasis, neuronal vulnerability, memory impairment, glucocorticoid negative feedback
- MeSH terms
- Animals, Calcium, Glucocorticoids, Hippocampus, Humans, Learning, Memory, Metaplasia, Models, Biological, Neuronal Plasticity, Stress, Physiological, Long-Term Potentiation
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