ArticlePloS one2012
Involvement of microglia activation in the lead induced long-term potentiation impairment.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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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
42 citing papers in PubMed, 108 citations in OpenAlex.
- Molecular Basis of Ferroptosis and Pyroptosis in Lead-Induced Neurotoxicity: A Narrative Review of Current Evidence and Therapeutic Implications.Biological trace element research · 2026Review
- Chronic Vanadium Exposure Promotes Aggregation of Alpha-Synuclein, Tau and Amyloid Beta in Mouse Brain.Journal of neurochemistry · 2025Article
- Hypertension Increases Susceptibility to Lead-Induced Microglial Polarization via ANT1-Mediated Mitochondrial DNA/cGAS/STING Signaling.Research (Washington, D.C.) · 2025Article
- The role of microglia in neuronal and cognitive function during high altitude acclimatization.Scientific reports · 2024Article
- Physical exercise regulates microglia in health and disease.Frontiers in neuroscience · 2024Review
- Metallothionein expression in the central nervous system in response to chronic heavy metal exposure: possible neuroprotective mechanism.Environmental geochemistry and health · 2023Article
- Common and Trace Metals in Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2023Review
- Microglia and Astroglia-The Potential Role in Neuroinflammation Induced by Pre- and Neonatal Exposure to Lead (Pb).International journal of molecular sciences · 2023Article
- Article
- Microglial Activation in Metal Neurotoxicity: Impact in Neurodegenerative Diseases.BioMed research international · 2023Review
- Effects of co-exposure to lead and manganese on learning and memory deficits.Journal of environmental sciences (China) · 2022Article
- Antiviral Activities of Asarones and Rhizomes ofViruses · 2022Article
- Lead Exposure in Developmental Ages Promotes Aβ Accumulation by Disturbing Aβ Transportation in Blood-Cerebrospinal Fluid Barrier/Blood-Brain Barriers and Impairing Aβ Clearance in the Liver.Biological trace element research · 2022Article
- Alleviating Effects of Black Soybean Peptide on Oxidative Stress Injury Induced by Lead in PC12 Cells via Keap1/Nrf2/TXNIP Signaling Pathway.Nutrients · 2022Article
- Exposure of metal toxicity in Alzheimer's disease: An extensive review.Frontiers in pharmacology · 2022Review
- Building a Network of Adverse Outcome Pathways (AOPs) Incorporating the Tau-Driven AOP Toward Memory Loss (AOP429).Journal of Alzheimer's disease reports · 2022Review
- Maternal Lead Exposure Impairs Offspring Learning and Memory via Decreased GLUT4 Membrane Translocation.Frontiers in cell and developmental biology · 2021Article
- MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY.Advances in neurotoxicology · 2021Article
- Modulatory Effects of PbEnvironmental toxicology and chemistry · 2020Article
- Developmental exposure to PbChemosphere · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure of Lead (Pb), a known neurotoxicant, can impair spatial learning and memory probably via impairing the hippocampal long-term potentiation (LTP) as well as hippocampal neuronal injury. Activation of hippocampal microglia also impairs spatial learning and memory. Thus, we raised the hypothesis that activation of microglia is involved in the Pb exposure induced hippocampal LTP impairment and neuronal injury. To test this hypothesis and clarify its underlying mechanisms, we investigated the Pb-exposure on the microglia activation, cytokine release, hippocampal LTP level as well as neuronal injury in in vivo or in vitro model. The changes of these parameters were also observed after pretreatment with minocycline, a microglia activation inhibitor. Long-term low dose Pb exposure (100 ppm for 8 weeks) caused significant reduction of LTP in acute slice preparations, meanwhile, such treatment also significantly increased hippocampal microglia activation as well as neuronal injury. In vitro Pb-exposure also induced significantly increase of microglia activation, up-regulate the release of cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and inducible nitric oxide synthase (iNOS) in microglia culture alone as well as neuronal injury in the co-culture with hippocampal neurons. Inhibiting the microglia activation with minocycline significantly reversed the above-mentioned Pb-exposure induced changes. Our results showed that Pb can cause microglia activation, which can up-regulate the level of IL-1β, TNF-α and iNOS, these proinflammatory factors may cause hippocampal neuronal injury as well as LTP deficits.
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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.