ArticleBrain, behavior, and immunity2012
Glucocorticoids mediate stress-induced priming of microglial pro-inflammatory responses.
Article in Brain, behavior, and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
165 citing papers in PubMed, 1 synthesis or guideline pooled it, 295 citations in OpenAlex.
- Gene expression signatures of response to fluoxetine treatment: systematic review and meta-analyses.Molecular psychiatry · 2025Pooled it
- Trial
- A neuroimmune framework for understanding adolescent stress and risk of alcohol misuse.Brain, behavior, & immunity - health · 2026Review
- Repeated restraint stress-induced increase in post-surgical somatosensory hypersensitivity and affective responding is mediated by β-adrenergic receptor activation and spinal NLRP3-IL1β signalling in male rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- A multi-omic atlas in the African turquoise killifish reveals increased glucocorticoid signaling as a hallmark of brain aging.bioRxiv : the preprint server for biology · 2026Article
- A Flupirtine Benzyl Carbamate Improves Neurocognitive Deficits and Molecular Pathology in theCells · 2026Article
- L-fucose administration ameliorates chronic social defeat stress-induced depressive-like behaviors by restoring GDP-fucose biosynthetic activation and core fucosylation.Frontiers in immunology · 2026Article
- Persistent priming of hypothalamic microglia is associated with sensitization of the hypothalamic-pituitary-adrenal axis to acute stress, hyperactivity and behavioral response disruption in male rats.Frontiers in immunology · 2026Article
- Prenatal stress shapes discrete responses during early recovery from repeated adult stress.Frontiers in cellular neuroscience · 2026Article
- Anxiolytic Effects ofInternational journal of general medicine · 2026Article
- Rethinking Corticosteroid Therapy in Pediatric Neurology.Journal of inflammation research · 2026Article
- Corticotropin-releasing factor (CRF) in brain aging: from mitochondrial dysfunction to inflammaging.Frontiers in aging neuroscience · 2026Review
- From Stress to Substance Use Disorders: The Expanding Role of Microglia-Astrocyte Crosstalk in Neuroimmune and Glutamate Alterations in the Nucleus Accumbens.International journal of molecular sciences · 2025Review
- Re-Examination of Inflammation in Major Depressive Disorder: Bridging Systemic and Neuroinflammatory Insights.Biomolecules · 2025Review
- Microglia sensing of peripheral signals that bridge the brain and body.Molecular neurodegeneration · 2025Review
- Differential Responses of Human iPSC-Derived Microglia to Stimulation with Diverse Inflammogens.Cells · 2025Article
- Review of the Effects of Lifestyle Modification on Parkinson's Disease.American journal of lifestyle medicine · 2025Article
- Smaller hippocampal tail volume is associated with plasma CCL11 levels in patients with major depressive disorder.Psychological medicine · 2025Article
- Flavins and Flavoproteins in the Neuroimmune Landscape of Stress Sensitization and Major Depressive Disorder.Journal of inflammation research · 2025Review
- Enduring memory consequences of early-life stress / adversity: Structural, synaptic, molecular and epigenetic mechanisms.Neurobiology of stress · 2024Review
105 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Acute and chronic stress sensitizes or "primes" the neuroinflammatory response to a subsequent pro-inflammatory challenge. While prior evidence shows that glucocorticoids (GCs) play a pivotal role in stress-induced potentiation of neuroinflammatory responses, it remains unclear whether stress-induced GCs sensitize the response of key CNS immune substrates (i.e. microglia) to pro-inflammatory stimuli. An ex vivo approach was used to address this question. Here, stress-induced GC signaling was manipulated in vivo and hippocampal microglia challenged with the pro-inflammatory stimulus LPS ex vivo. Male Sprague-Dawley rats were either pretreated in vivo with the GC receptor antagonist RU486 or adrenalectomized (ADX). Animals were then exposed to an acute stressor (inescapable tailshock; IS) and 24 h later hippocampal microglia were isolated and challenged with LPS to probe for stress-induced sensitization of pro-inflammatory responses. Prior exposure to IS resulted in a potentiated pro-inflammatory cytokine response (e.g. IL-1β gene expression) to LPS in isolated microglia. Treatment in vivo with RU486 and ADX inhibited or completely blocked this IS-induced sensitization of the microglial pro-inflammatory response. The present results suggest that stress-induced GCs function to sensitize the microglial pro-inflammatory response (IL-1β, IL-6, NFκBIα) to immunologic challenges.
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What OpenQuestion holds
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.