ArticleProceedings of the National Academy of Sciences of the United States of America2008
Acute corticosterone treatment is sufficient to induce anxiety and amygdaloid dendritic hypertrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers.
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Who cites it
175 citing papers in PubMed, 404 citations in OpenAlex.
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- Exogenous glucocorticoids decrease subgenual cingulate activity evoked by sadness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013Trial
- Acute hydrocortisone treatment increases anxiety but not fear in healthy volunteers: a fear-potentiated startle study.Biological psychiatry · 2011Trial
- Attenuation of amygdala atrophy with lamotrigine in patients receiving corticosteroid therapy.Journal of clinical psychopharmacology · 2009Trial
- Frequency of bullying modulates amygdala response during social exclusion in participants with non-suicidal self-injury.European child & adolescent psychiatry · 2026Article
- Sgk1 upregulation in hippocampus-projecting amygdala neurons underlies the delayed onset of PTSD-like avoidance behavior.Nature communications · 2026Article
- Dose-dependent anxiolytic and antidepressant-like effects of chronic oxytocin in corticosterone-induced female mouse model of anxiety and depression.Biochemistry and biophysics reports · 2026Article
- A single glucocorticoid response element regulates sociability in a sex-specific manner.Molecular psychiatry · 2026Article
- Unpredictable stress boosts perceptual learning and alters glucocorticoid and norepinephrine receptors in rats' dorsal hippocampus.Translational psychiatry · 2025Article
- Sex differences in resilience at puberty depend upon divergent effects of a stress steroid at α4βδ GABABrain research · 2025Article
- Functional Movement Disorder: Evolving Mechanisms, Diagnostic Precision, and Personalized Multidisciplinary Care.Movement disorders clinical practice · 2025Review
- Stress-Responsive Neuronal Ensembles and β-Adrenergic Signaling in the Basolateral Amygdala Modulate the Infralimbic Cortical Activity and Govern the Delayed Stress-Induced Fear Extinction Deficit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Is neglect the first form of threat?Attachment & human development · 2025Review
- Consumption of the Prebiotic-Rich Chicory Taproot Contrasts the Cognitive and Motivational Consequences of Chronic Corticosterone Exposure and Modulates Gut Microbiota Composition in Mice.Biological psychiatry global open science · 2025Article
- Reduced Gene Dosage of the Psychiatric Risk GeneInternational journal of molecular sciences · 2025Article
- Regional brain structural alterations in reward and salience networks in asthma.Brain, behavior, and immunity · 2025Article
- Stk24 deficiency causes disrupted hippocampal neurogenesis and anxiety-like behavior in mice.Communications biology · 2025Article
- A Scoping Review of Corticosterone-Induced Changes in Ionotropic Glutamate Receptor Levels and Localization in the Rodent Brain: Implications for the Auditory System.Brain sciences · 2025Review
115 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
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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