Glucocorticoids Protect Against the Delayed Behavioral and Cellular Effects of Acute Stress on the Amygdala
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Background A single episode of acute immobilization stress has previously been shown to trigger a delayed onset of anxiety-like behavior and spinogenesis in the basolateral amygdala (BLA) of rats. Spurred on by a seemingly paradoxical observation in which even a modest increase in corticosterone (CORT), caused by a single vehicle injection before stress, could dampen the delayed effects of stress, we hypothesized a protective role for glucocorticoids against stress.Methods We tested this hypothesis by analyzing how manipulations in CORT levels modulate delayed increase in anxiety-like behavior of rats on the elevated plus-maze 10 days after acute stress. We also investigated the cellular correlates of different levels of anxiety under different CORT conditions by quantifying spine density on Golgi-stained BLA principal neurons.Results CORT in drinking water for 12 hours preceding acute stress prevented delayed increase in anxiety rather than exacerbating it. Conversely, vehicle injection failed to prevent the anxiogenic effect of stress in bilaterally adrenalectomized rats. However, when CORT was restored in adrenalectomized rats by injection, the delayed anxiogenic effect of stress was once again blocked. Finally, high and low anxiety states were accompanied by high and low levels of BLA spine density.Conclusions Our findings suggest that the presence of elevated levels of CORT at the time of acute stress confers protection against the delayed enhancing effect of stress on BLA synaptic connectivity and anxiety-like behavior. These observations are consistent with clinical reports on the protective effects of glucocorticoids against the development of posttraumatic symptoms triggered by traumatic stress.
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In animal models of traumatic stress-induced PTSD-like delayed anxiety and traumatic stress-induced spine synapse formation in basolateral amygdala, a timed elevation of glucocorticoids prevents these effects.
“For example, in several animal models of traumatic stress-induced PTSD-like delayed anxiety and (in one model) traumatic stress induced spine synapse formation in BlA, a timed elevation of glucocorticoids prevents these effect.”
From Neurobiological and Systemic Effects of Chronic Stress (2017) · cites this paper as [21]
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“For example, in several animal models of traumatic stressinduced PTSD-like delayed anxiety and (in one model) traumatic stress induced spine synapse formation in BlA, a timed elevation of glucocorticoids prevents these effect.(21) Data on human PTSD support a protective role for adequate glucocorticoid levels at time…”
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- Authors
- Rao, R. P., Anilkumar, S., McEwen, B. S., & Chattarji, S.
- Affiliations
- Tata Institute of Fundamental Research (IN)
- Rockefeller University (US)
- Corresponding author
- Chattarji, Sumantra
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2012-09
- Volume
- 72
- Issue
- 6
- Pages
- 466-475
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3753225
- OpenAlex
- W2044913415
- Cited by
- 131
- References
- 56
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 6 · 2023: 11 · 2022: 6 · 2021: 10 · 2020: 10 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 8 · 2015: 15 · 2014: 17 · 2013: 6 · 2012: 4
- FWCI
- 5.63
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Lightfighter Trust and National Institute of Mental Health (5P50 MH58911)
- 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
- glucocorticoids, corticosterone, acute immobilization stress, anxiety-like behavior, basolateral amygdala, spinogenesis, dendritic spine density, synaptic connectivity, adrenalectomy, post-traumatic stress, stress buffering
- MeSH terms
- Adrenalectomy, Amygdala, Analysis of Variance, Animals, Anxiety, Corticosterone, Disease Models, Animal, Glucocorticoids, Male, Restraint, Physical, Stress Disorders, Post-Traumatic, Stress, Psychological, Rats, Wistar, Dendritic Spines, Rats
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