ReviewBrain, behavior, and immunity2011
Stress- and glucocorticoid-induced priming of neuroinflammatory responses: potential mechanisms of stress-induced vulnerability to drugs of abuse.
Review in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
64 citing papers in PubMed, 118 citations in OpenAlex.
- Systemic inflammation enhances stimulant-induced striatal dopamine elevation in tobacco smokers.Brain, behavior, and immunity · 2022Trial
- Effects of ibudilast on central and peripheral markers of inflammation in alcohol use disorder: A randomized clinical trial.Addiction biology · 2022Trial
- Development of the Neuroimmune Modulator Ibudilast for the Treatment of Alcoholism: A Randomized, Placebo-Controlled, Human Laboratory Trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Trial
- Neuroprotective Effects of Carnosine Against Corticosterone-Induced Depression and Memory Impairment.Food science & nutrition · 2026Article
- 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
- Neutrophil Elastase (ELANE) as a Novel Neuroinflammatory Biomarker in Alcohol Use Disorder: Clinical Validation.Addiction biology · 2025Article
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- Prenatal substance exposure and infant neurodevelopment: a review of magnetic resonance imaging studies.Frontiers in human neuroscience · 2025Review
- Comprehensive Review of Chronic Stress Pathways and the Efficacy of Behavioral Stress Reduction Programs (BSRPs) in Managing Diseases.International journal of environmental research and public health · 2024Review
- Microglia in neuroimmunopharmacology and drug addiction.Molecular psychiatry · 2024Review
- Prenatal exposure to maternal disadvantage-related inflammatory biomarkers: associations with neonatal white matter microstructure.Translational psychiatry · 2024Article
- Early and recent exposure to adversity, TLR-4 stimulated inflammation, and diurnal cortisol in women with interstitial cystitis/bladder pain syndrome: A MAPP research network study.Brain, behavior, and immunity · 2023Article
- Anti-Inflammatory Therapy as a Promising Target in Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2023Review
- Early Life Stress, Neuroinflammation, and Psychiatric Illness of Adulthood.Advances in experimental medicine and biology · 2023Review
- Stress- and drug-induced neuroimmune signaling as a therapeutic target for comorbid anxiety and substance use disorders.Pharmacology & therapeutics · 2022Review
- Is the Neuroimmune System a Therapeutic Target for Opioid Use Disorder? A Systematic Review.Medical research archives · 2022Article
- Increased alcohol self-administration following repeated Toll-like receptor 3 agonist treatment in male and female rats.Pharmacology, biochemistry, and behavior · 2022Article
- The transcription factor CCAAT/enhancer-binding protein β in spinal microglia contributes to pre-operative stress-induced prolongation of postsurgical pain.Molecular pain · 2022Article
4 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Stress and stress-induced glucocorticoids (GCs) sensitize drug abuse behavior as well as the neuroinflammatory response to a subsequent pro-inflammatory challenge. Stress also predisposes or sensitizes individuals to develop substance abuse. There is an emerging evidence that glia and glia-derived neuroinflammatory mediators play key roles in the development of drug abuse. Drugs of abuse such as opioids, psychostimulants, and alcohol induce neuroinflammatory mediators such as pro-inflammatory cytokines (e.g. interleukin (IL)-1β), which modulate drug reward, dependence, and tolerance as well as analgesic properties. Drugs of abuse may directly activate microglial and astroglial cells via ligation of Toll-like receptors (TLRs), which mediate the innate immune response to pathogens as well as xenobiotic agents (e.g. drugs of abuse). The present review focuses on understanding the immunologic mechanism(s) whereby stress primes or sensitizes the neuroinflammatory response to drugs of abuse and explores whether stress- and GC-induced sensitization of neuroimmune processes predisposes individuals to drug abuse liability and the role of neuroinflammatory mediators in the development of drug addiction.
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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.