Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex
Open accessAbstract
The hippocampus provided the gateway into much of what we have learned about stress and brain structural and functional plasticity, and this initial focus has expanded to other interconnected brain regions, such as the amygdala and prefrontal cortex. Starting with the discovery of adrenal steroid, and later, estrogen receptors in the hippocampal formation, and subsequent discovery of dendritic and spine synapse remodeling and neurogenesis in the dentate gyrus, mechanistic studies have revealed both genomic and rapid non-genomic actions of circulating steroid hormones in the brain. Many of these actions occur epigenetically and result in ever-changing patterns of gene expression, in which there are important sex differences that need further exploration. Moreover, glucocorticoid and estrogen actions occur synergistically with an increasing number of cellular mediators that help determine the qualitative nature of the response. The hippocampus has also been a gateway to understanding lasting epigenetic effects of early-life experiences. These findings in animal models have resulted in translation to the human brain and have helped change thinking about the nature of brain malfunction in psychiatric disorders and during aging, as well as the mechanisms of the effects of early-life adversity on the brain and the body.
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Chronically elevated glucocorticoid levels induce remodeling of hippocampus, amygdala, and mPFC.
“Chronically elevated glucocorticoid levels, in turn, are known to induce remodeling of the hippocampus, amygdala, and mPFC [71]”
From Trauma, PTSD, and the Developing Brain (2017) · cites this paper as [71]
The Neural Structural Remodeling section (page unavailable) says much of the described remodeling is mediated through glucocorticoid-receptor-dependent gene expression. The Traumatic Stress Effects section links elevated corticosterone to amygdala dendritic changes, but its direct corticosterone example uses a single bolus. These passages support a role for glucocorticoids in remodeling, not the broader assertion that chronically elevated levels themselves induce remodeling in all three named regions. (LLM, conf=0.85)
Experimental — accuracy not yet measuredChanges in the structure and function of neurons may occur under chronic stress and lead to the occurrence of MDD.
“It has been proved that the changes in the structure and function of neurons may occur under the chronic stress and lead to the occurrence of MDD. 37 , 38”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [37]
The Neural Structural Remodeling and PFC sections report that chronic stress changes neuronal structure, and the Translation to the Human Hippocampus section says depression may persist when resilience is lacking. The paper does not establish that those neuronal changes cause the onset of major depressive disorder; it describes stress-related remodeling as largely reversible and often adaptive. (LLM, conf=0.84)
Experimental — accuracy not yet measuredFindings in mood disorders reveal alterations at the levels of intracellular signaling, gene expression, neurotrophic factors, neurogenesis, neuroinflammation, excitatory and inhibitory neurotransmission, and synaptic number and function in several brain regions implicated in depression.
“These findings reveal alterations at the levels of intracellular signaling, gene expression, neurotrophic factors, neurogenesis, neuroinflammation, excitatory and inhibitory neurotransmission, and synaptic number and function, and have been described in several brain regions implicated in depression 13-22 .”
From Neuroplasticity in cognitive and psychological mechanisms of depression: an integrative model (2020) · cites this paper as [18]
The sections on hippocampal involvement in mood disorders and identification of new gene candidates discuss neurogenesis, neurotrophic factors, gene expression, inflammatory signaling, and synaptic remodeling in relation to stress or depression; Future Directions also describes intracellular signaling changes. The copy does not establish the full list as findings in mood disorders across several depression-related regions: its discussion of excitatory–inhibitory balance, for example, concerns plasticity more generally. No page numbers are available in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredExaggerated fear is a core symptom of clinical anxiety and fear responding is closely linked to stress.
“Exaggerated fear is a core symptom of clinical anxiety and fear responding is closely linked to stress (Maren and Holmes, 2016;McEwen et al., 2016;Raio and Phelps, 2015), which (as described in Sections VI.G. and VII.H.) is tightly intertwined with gut-brain axis function.”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as McEwen et al., 2016
The sections on structural remodeling in the amygdala and traumatic stress effects link stress to increased anxiety and altered fear conditioning. The human-amygdala section discusses chronic anxiety disorders, but the available passages do not say that exaggerated fear is a core symptom of clinical anxiety. Page numbers were not supplied. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAccompanying behavioral changes in chronic stress models are marked physiological and structural alterations in the amygdala, hippocampus, and prefrontal cortex that are similar to those seen in major depressive disorder.
“Accompanying these behavioral changes are marked physiological and structural alterations, not only in the amygdala and hippocampus but, importantly, the PFC [98,99], that are similar to those seen in MDD.”
From Prefrontal cortex and depression (2022) · cites this paper as [99]
The section on sex differences after puberty reports depressive-like behavior alongside chronic-stress-induced remodeling of the hippocampus, PFC, and amygdala; the PFC section also describes structural remodeling after chronic stress. The copy discusses findings in depressed people for the hippocampus, but the passages do not establish that the alterations across all three regions are similar to those seen in MDD. Page numbers were not available in the indexed passages. (LLM, conf=0.82)
Experimental — accuracy not yet measured
In rodents, the most abundant and consistent changes in chronic stress models are in the medial prefrontal cortex, including anterior cingulate, prelimbic, and infralimbic regions, with somewhat more variable, mixed direction effects in the orbitofrontal cortex.
“In rodents, the most abundant and consistent changes are in the mPFC (anterior cingulate, prelimbic and infralimbic) with somewhat more variable, mixed direction effects in the OFC (Fig. 3, top left-hand panel).”
From Prefrontal cortex and depression (2022) · cites this paper as [99]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredStudies of chronic stress or glucocorticoid exposure in adult animals show effects on frontolimbic circuitry including dendritic atrophy of mPFC and hippocampus, and expansion of basolateral amygdala.
“Studies of chronic stress or glucocorticoid exposure in adult animals show notable effects on frontolimbic circuitry including dendritic atrophy of the mPFC and hippocampus, and expansion of the basolateral amygdala [71].”
From Trauma, PTSD, and the Developing Brain (2017) · cites this paper as [71]
The effect of stress on neuronal morphology and functions varies across brain regions.
“In recent years, it has become increasingly clear that the effect of stress on neuronal morphology and functions varies across brain regions (53–56).”
From Chronic Stress Remodels Synapses in an Amygdala Circuit-Specific Manner (2019) · cites this paper as [56]
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- Authors
- McEwen, B. S., Nasca, C., & Gray, J. D.
- Affiliations
- Rockefeller University (US)
- Venue
- Neuropsychopharmacology
- Published
- 2015-06-16
- Volume
- 41
- Issue
- 1
- Pages
- 3-23
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC4677120
- OpenAlex
- W756325778
- Cited by
- 1,574
- References
- 218
- Citations by year
- 2026: 185 · 2025: 223 · 2024: 172 · 2023: 158 · 2022: 165 · 2021: 181 · 2020: 152 · 2019: 126 · 2018: 104 · 2017: 61 · 2016: 40 · 2015: 6
- FWCI
- 5.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Foundation for Suicide Prevention
- Hope for Depression Research Foundation
- National Institutes of Health (MH41256)
- National Institute of Mental Health (R01 MH41256, F32MH102065, R01MH041256)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- stress, hippocampus, amygdala, prefrontal cortex, neuroplasticity, dendritic remodeling, synaptic remodeling, dentate gyrus neurogenesis, glucocorticoids, estrogen receptor, non-genomic steroid action, epigenetics, sex differences, childhood adversity, early life experience, mental illness, brain aging
- MeSH terms
- Amygdala, Animals, Hippocampus, Humans, Nerve Net, Neuronal Plasticity, Neurons, Stress, Psychological, Prefrontal Cortex
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