Cited by 409Stress Responses and CortisolMemory and Neural MechanismsNeuroscience and Neuropharmacology Research

Acute corticosterone treatment is sufficient to induce anxiety and amygdaloid dendritic hypertrophy

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Mitra, Rupshi, Sapolsky, Robert M.·2008·Proceedings of the National Academy of Sciences

Abstract

Stress is known to induce dendritic hypertrophy in the basolateral amygdala (BLA) and to enhance anxiety. Stress also leads to secretion of glucocorticoids (GC), and the BLA has a high concentration of glucocorticoid receptors. This raises the possibility that stress-induced elevation in GC secretion might directly affect amygdaloid neurons. To address the possible effects of GC on neurons of amygdala and on anxiety, we used rats treated either acutely with a single dose or chronically with 10 daily doses of high physiological levels of corticosterone (the rat-specific glucocorticoid). Behavior and morphological changes in neurons of BLA were measured 12 days after the initiation of treatment in both groups. A single acute dose of corticosterone was sufficient to induce dendritic hypertrophy in the BLA and heightened anxiety, as measured on an elevated plus maze. Moreover, this form of dendritic hypertrophy after acute treatment was of a magnitude similar to that caused by chronic treatment. Thus, plasticity of BLA neurons is sufficiently sensitive so as to be saturated by a single day of stress. The effects of corticosterone were specific to anxiety, as neither acute nor chronic treatment caused any change in conditioned fear or in general locomotor activity in these animals.

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Crossref · 10.1073/pnas.0705615105

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  • Neuronal and synaptic remodeling in BLA PNs, along with enhanced glutamatergic transmission, has been repeatedly associated with the negative consequence of stress.

    “Neuronal and synaptic remodeling in BLA PNs, along with enhanced glutamatergic transmission, has been repeatedly associated with the negative consequence of stress (14,33,34,40), and prevention of these changes is paralleled by a protection against stress-induced increases in anxiety-like behavior (26,41).”
  • Repeated high-dose glucocorticoid treatment mimics chronic stress and induces dendritic lengthening in basolateral amygdala.

    “Yet, repeated high dose glucocorticoids treatment mimics chronic stress and induces dendritic lengthening in BlA.”

    From Neurobiological and Systemic Effects of Chronic Stress (2017) · cites this paper as [36]

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Authors
Mitra, R., & Sapolsky, R. M.
Affiliations
  • Stanford University (US)
  • Rockefeller University (US)
Venue
Proceedings of the National Academy of Sciences
Published
2008-04-08
Volume
105
Issue
14
Pages
5573-5578
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2141747860
Cited by
409
References
61
Citations by year
2026: 9 · 2025: 15 · 2024: 16 · 2023: 12 · 2022: 23 · 2021: 28 · 2020: 19 · 2019: 26 · 2018: 25 · 2017: 20 · 2016: 39 · 2015: 19 · 2014: 26 · 2013: 23 · 2012: 29
FWCI
12.05
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • U.S. Public Health Service (R01 AGO20633)
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
corticosterone, glucocorticoids, anxiety, basolateral amygdala, neuroplasticity, stress, glucocorticoid receptor, elevated plus maze, fear conditioning, locomotor activity
MeSH terms
Amygdala, Animals, Anxiety, Corticosterone, Dendrites, Hypertrophy, Neuronal Plasticity, Stress, Physiological, Rats

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