ArticleJournal of neuroinflammation2013
Activation of microglial cells triggers a release of brain-derived neurotrophic factor (BDNF) inducing their proliferation in an adenosine A2A receptor-dependent manner: A2A receptor blockade prevents BDNF release and proliferation of microglia.
Article in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
113 citing papers in PubMed, 2 syntheses or guidelines pooled it, 223 citations in OpenAlex.
- Gene expression signatures of response to fluoxetine treatment: systematic review and meta-analyses.Molecular psychiatry · 2025Pooled it
- Cytokines and Brain-Derived Neurotrophic Factor as Biomarkers of Cognitive Impairment Related to Breast Cancer and Its Treatments: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Regular intake of caffeinated but not decaffeinated coffee attenuates behavioral modifications in mice subject to chronic unpredictable stress.Neurobiology of stress · 2026Article
- Targeted inhibition of the BDNF/AKT/mTOR pathway in the inferior colliculus ameliorates salicylate-induced tinnitus in rats.iScience · 2026Article
- Article
- Putative mechanisms of caffeine as a neuroprotectant in preterm infants.Pediatric research · 2026Review
- BDNF insufficiency exacerbates ALS progression.Cell reports. Medicine · 2026Article
- Editorial: Evaluating efficacy and outcomes in neonatal HIE treatment: A global perspective.Frontiers in pediatrics · 2026Article
- Adenosine A2A signaling in mood disorders: How far have we come?IBRO neuroscience reports · 2025Article
- The systemic costs of hematopoietic stem cell aging.Development (Cambridge, England) · 2025Review
- The orexin/hypocretin system in dementia-related neurological disorders: a double-edged sword in cognitive impairment.Psychopharmacology · 2025Review
- Molecular Mechanisms Underlying Neuroinflammation Intervention with Medicinal Plants: A Critical and Narrative Review of the Current Literature.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Microglia's Phenotypic Heterogeneity in Pain Pathogenesis and Electroacupuncture Analgesia: Mechanisms and Therapeutic Potential.Journal of pain research · 2025Review
- Filbertone-Induced Nrf2 Activation Ameliorates Neuronal Damage via Increasing BDNF Expression.Neurochemical research · 2024Article
- Glia-related Acute Effects of Risperidone and Haloperidol in Hippocampal Slices and Astrocyte Cultures from Adult Wistar Rats: A Focus on Inflammatory and Trophic Factor Release.Neurochemical research · 2024Article
- Toward discovering a novel family of peptides targeting neuroinflammatory states of brain microglia and astrocytes.Journal of neurochemistry · 2024Article
- Adenosine and adenosine receptors in metabolic imbalance-related neurological issues.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Review
- Modulation of Oxidative Stress and Neuroinflammation by Cannabidiol (CBD): Promising Targets for the Treatment of Alzheimer's Disease.Current issues in molecular biology · 2024Review
- Article
- Recent advances in the crosstalk between the brain-derived neurotrophic factor and glucocorticoids.Frontiers in endocrinology · 2024Review
53 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBrain-derived neurotrophic factor (BDNF) has been shown to control microglial responses in neuropathic pain. Since adenosine A2A receptors (A2ARs) control neuroinflammation, as well as the production and function of BDNF, we tested to see if A2AR controls the microglia-dependent secretion of BDNF and the proliferation of microglial cells, a crucial event in neuroinflammation.
methodsMurine N9 microglial cells were challenged with lipopolysaccharide (LPS, 100 ng/mL) in the absence or in the presence of the A2AR antagonist, SCH58261 (50 nM), as well as other modulators of A2AR signaling. The BDNF cellular content and secretion were quantified by Western blotting and ELISA, A2AR density was probed by Western blotting and immunocytochemistry and cell proliferation was assessed by BrdU incorporation. Additionally, the A2AR modulation of LPS-driven cell proliferation was also tested in primary cultures of mouse microglia.
resultsLPS induced time-dependent changes of the intra- and extracellular levels of BDNF and increased microglial proliferation. The maximal LPS-induced BDNF release was time-coincident with an LPS-induced increase of the A2AR density. Notably, removing endogenous extracellular adenosine or blocking A2AR prevented the LPS-mediated increase of both BDNF secretion and proliferation, as well as exogenous BDNF-induced proliferation.
conclusionsWe conclude that A2AR activation plays a mandatory role controlling the release of BDNF from activated microglia, as well as the autocrine/paracrine proliferative role of BDNF.
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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.