ArticleCellular and molecular neurobiology2019
Resetting the Stress System with a Mifepristone Challenge.
Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Efficacy and Safety of Mifepristone in the Treatment of Male US Veterans With Posttraumatic Stress Disorder: A Phase 2a Randomized Clinical Trial.JAMA network open · 2023Trial
- Correlation between clinical features of acute episode of major depressive disorder and hypothalamic-pituitary-adrenal axis (HPA) function: a cross-sectional study.BMC psychiatry · 2026Article
- Alk-Fam150b (augmentor α) expression in the paraventricular nucleus of the mouse hypothalamus at molecular resolution, and its sensitivity to acute stress.Journal of neuroendocrinology · 2026Article
- Sex and Age Differences in Glucocorticoid Signaling After an Aversive Experience in Mice.Cells · 2024Article
- Effect of Mifepristone on Migration and Proliferation of Oral Cancer Cells.International journal of molecular sciences · 2024Article
- The cortisol switch between vulnerability and resilience.Molecular psychiatry · 2024Review
- Three Prospective Case Studies Examining Mifepristone's Efficacy in Patients with Treatment-Resistant PTSD.Case reports in psychiatry · 2024Article
- Coping with the multifaceted and multifunctional role of cortisol in the brain.Neuroscience applied · 2024Review
- Harnessing PROTAC technology to combat stress hormone receptor activation.Nature communications · 2023Article
- Alterations of monoamine neurotransmitters, HPA-axis hormones, and inflammation cytokines in reserpine-induced hyperalgesia and depression comorbidity rat model.BMC psychiatry · 2022Article
- Brain mineralocorticoid and glucocorticoid receptor balance in neuroendocrine regulation and stress-related psychiatric etiopathologies.Current opinion in endocrine and metabolic research · 2022Review
- Corticosteroid sensitization drives opioid addiction.Molecular psychiatry · 2022Article
- Mineralocorticoid receptor and glucocorticoid receptor work alone and together in cell-type-specific manner: Implications for resilience prediction and targeted therapy.Neurobiology of stress · 2022Article
- Forced swim stressor: Trends in usage and mechanistic consideration.The European journal of neuroscience · 2022Review
- Alcohol dependence and withdrawal increase sensitivity of central amygdalar GABAergic synapses to the glucocorticoid receptor antagonist mifepristone in male rats.Neurobiology of disease · 2022Article
- Glucocorticoid receptor modulators decrease alcohol self-administration in male rats.Neuropharmacology · 2021Article
- The selective glucocorticoid receptor antagonist CORT125281 has tissue-specific activity.The Journal of endocrinology · 2020Article
- Insights into the Therapeutic Potential of Glucocorticoid Receptor Modulators for Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Glucocorticoids mediate stress induction of the alarmin HMGB1 and reduction of the microglia checkpoint receptor CD200R1 in limbic brain structures.Brain, behavior, and immunity · 2019Article
- Repression of the Glucocorticoid Receptor Increases Hypoxic-Ischemic Brain Injury in the Male Neonatal Rat.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Psychotic depression is characterized by elevated circulating cortisol, and high daily doses of the glucocorticoid/progesterone antagonist mifepristone for 1 week are required for significant improvement. Using a rodent model, we find that such high doses of mifepristone are needed because the antagonist is rapidly degraded and poorly penetrates the blood-brain barrier, but seems to facilitate the entry of cortisol. We also report that in male C57BL/6J mice, after a 7-day treatment with a high dose of mifepristone, basal blood corticosterone levels were similar to that of vehicle controls. This is surprising because after the first mifepristone challenge, corticosterone remained elevated for about 16 h, and then decreased towards vehicle control levels at 24 h. At that time, stress-induced corticosterone levels of the 1xMIF were sevenfold higher than the 7xMIF group, the latter response being twofold lower than controls. The 1xMIF mice showed behavioral hyperactivity during exploration of the circular hole board, while the 7xMIF mice rather engaged in serial search patterns. To explain this rapid reset of corticosterone secretion upon recurrent mifepristone administration, we suggest the following: (i) A rebound glucocorticoid feedback after cessation of mifepristone treatment. (ii) Glucocorticoid agonism in transrepression and recruitment of cell-specific coregulator cocktails. (iii) A more prominent role of brain MR function in control of stress circuit activity. An overview table of neuroendocrine MIF effects is provided. The data are of interest for understanding the mechanistic underpinning of stress system reset as treatment strategy for stress-related diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.