ArticleFrontiers in cellular neuroscience2015
Prenatal stress is a vulnerability factor for altered morphology and biological activity of microglia cells.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Stress and neuroinflammation: a systematic review of the effects of stress on microglia and the implications for mental illness.Psychopharmacology · 2016Pooled it
- Prenatal stress shapes discrete responses during early recovery from repeated adult stress.Frontiers in cellular neuroscience · 2026Article
- Microglia as critical mediators linking perinatal immune stress to mental health trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Effects of gestational intermittent hypoxia on the respiratory system: A tale of the placenta, fetus, and developing offspring.Journal of sleep research · 2025Review
- Perinatal Psychoneuroimmunology of Prenatal Stress and Its Effects on Fetal and Postnatal Brain Development.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Developmental functions of microglia: Impact of psychosocial and physiological early life stress.Neuropharmacology · 2024Review
- Mental disorders after myocardial infarction: potential mediator role for chemokines in heart-brain interaction?Journal of geriatric cardiology : JGC · 2024Article
- Embers of the Past: Early Childhood Traumas Interact with Variation inInternational journal of molecular sciences · 2024Article
- B cells and the stressed brain: emerging evidence of neuroimmune interactions in the context of psychosocial stress and major depression.Frontiers in cellular neuroscience · 2024Review
- Article
- Characterizing the neuroimmune environment of offspring in a novel model of maternal allergic asthma and particulate matter exposure.Journal of neuroinflammation · 2023Article
- Article
- Daytime Light Deficiency Leads to Sex- and Brain Region-Specific Neuroinflammatory Responses in a Diurnal Rodent.Cellular and molecular neurobiology · 2023Article
- Fetal hypoxia results in sex- and cell type-specific alterations in neonatal transcription in rat oligodendrocyte precursor cells, microglia, neurons, and oligodendrocytes.Cell & bioscience · 2023Article
- Inhibition of Microglial GSK3β Activity Is Common to Different Kinds of Antidepressants: A Proposal for an In Vitro Screen to Detect Novel Antidepressant Principles.Biomedicines · 2023Review
- The role of microglia in neuropsychiatric disorders and suicide.European archives of psychiatry and clinical neuroscience · 2022Review
- Design, Synthesis, Biological Evaluation, and Computational Studies of Novel Ureidopropanamides as Formyl Peptide Receptor 2 (FPR2) Agonists to Target the Resolution of Inflammation in Central Nervous System Disorders.Journal of medicinal chemistry · 2022Article
- The Impact of Maternal Antioxidants on Prenatal Stress Effects on Offspring Neurobiology and Behavior.The Yale journal of biology and medicine · 2022Article
- Serum CC Chemokines as Potential Biomarkers for the Diagnosis of Major Depressive Disorder.Psychology research and behavior management · 2022Article
- Research Progress on the Role of Microglia Membrane Proteins or Receptors in Neuroinflammation and Degeneration.Frontiers in cellular neuroscience · 2022Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several lines of evidence suggest that the dysregulation of the immune system is an important factor in the development of depression. Microglia are the resident macrophages of the central nervous system and a key player in innate immunity of the brain. We hypothesized that prenatal stress (an animal model of depression) as a priming factor could affect microglial cells and might lead to depressive-like disturbances in adult male rat offspring. We investigated the behavioral changes (sucrose preference test, Porsolt test), the expression of C1q and CD40 mRNA and the level of microglia (Iba1 positive) in 3-month-old control and prenatally stressed male offspring rats. In addition, we characterized the morphological and biochemical parameters of potentially harmful (NO, iNOS, IL-1β, IL-18, IL-6, TNF-α, CCL2, CXCL12, CCR2, CXCR4) and beneficial (insulin-like growth factor-1 (IGF-1), brain derived neurotrophic factor (BDNF)) phenotypes in cultures of microglia obtained from the cortices of 1-2 days old control and prenatally stressed pups. The adult prenatally stressed rats showed behavioral (anhedonic- and depression-like) disturbances, enhanced expression of microglial activation markers and an increased number of Iba1-immunopositive cells in the hippocampus and frontal cortex. The morphology of glia was altered in cultures from prenatally stressed rats, as demonstrated by immunofluorescence microscopy. Moreover, in these cultures, we observed enhanced expression of CD40 and MHC II and release of pro-inflammatory cytokines, including IL-1β, IL-18, TNF-α and IL-6. Prenatal stress significantly up-regulated levels of the chemokines CCL2, CXCL12 and altered expression of their receptors, CCR2 and CXCR4 while IGF-1 production was suppressed in cultures of microglia from prenatally stressed rats. Our results suggest that prenatal stress may lead to excessive microglia activation and contribute to the behavioral changes observed in depression in adulthood.
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