ArticlePloS one2015
Presynaptic mechanisms of lead neurotoxicity: effects on vesicular release, vesicle clustering and mitochondria number.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Caffeic Acid Mitigates Behavioral and Biochemical Alterations in Lead-induced Neurotoxicity in Rats With Possible Involvement of TFEB.Neurotoxicity research · 2026Article
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- Tracing the threads: How toxic metals contribute to neurodegeneration.IBRO neuroscience reports · 2026Review
- Evaluation of Heavy Metals and Essential Minerals in the Hair of Children with Autism Spectrum Disorder and Their Association with Symptom Severity.Biological trace element research · 2025Article
- Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.Acta neuropathologica communications · 2023Article
- Behavioral and Synaptic Phenotypes of FemaleAntioxidants (Basel, Switzerland) · 2022Article
- Alpha-Lipoic Acid Attenuates Cadmium- and Lead-Induced Neurotoxicity by Inhibiting Both Endoplasmic-Reticulum Stress and Activation of Fas/FasL and Mitochondrial Apoptotic Pathways in Rat Cerebral Cortex.Neurotoxicity research · 2021Article
- MOLECULAR MECHANISMS OF LEAD NEUROTOXICITY.Advances in neurotoxicology · 2021Article
- Methylphenidate and Rosmarinus officinalis improves cognition and regulates inflammation and synaptic gene expression in AlClMolecular biology reports · 2020Article
- Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats.International journal of molecular sciences · 2020Article
- Long-term consequences of early postnatal lead exposure on hippocampal synaptic activity in adult mice.Brain and behavior · 2019Article
- Development of the Adverse Outcome Pathway (AOP): Chronic binding of antagonist to N-methyl-d-aspartate receptors (NMDARs) during brain development induces impairment of learning and memory abilities of children.Toxicology and applied pharmacology · 2018Article
- From the Cover: 7,8-Dihydroxyflavone Rescues Lead-Induced Impairment of Vesicular Release: A Novel Therapeutic Approach for Lead Intoxicated Children.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Environmental Pollutants and Neurodevelopment: Review of Benefits From Closure of a Coal-Burning Power Plant in Tongliang, China.Global pediatric health · 2017Article
- Chronic early life lead (PbBMC pharmacology & toxicology · 2016Article
- Defining potential roles of Pb(2+) in neurotoxicity from a calciomics approach.Metallomics : integrated biometal science · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Childhood lead (Pb2+) intoxication is a global public health problem and accounts for 0.6% of the global burden of disease associated with intellectual disabilities. Despite the recognition that childhood Pb2+ intoxication contributes significantly to intellectual disabilities, there is a fundamental lack of knowledge on presynaptic mechanisms by which Pb2+ disrupts synaptic function. In this study, using a well-characterized rodent model of developmental Pb2+ neurotoxicity, we show that Pb2+ exposure markedly inhibits presynaptic vesicular release in hippocampal Schaffer collateral-CA1 synapses in young adult rats. This effect was associated with ultrastructural changes which revealed a reduction in vesicle number in the readily releasable/docked vesicle pool, disperse vesicle clusters in the resting pool, and a reduced number of presynaptic terminals with multiple mitochondria with no change in presynaptic calcium influx. These studies provide fundamental knowledge on mechanisms by which Pb2+ produces profound inhibition of presynaptic vesicular release that contribute to deficits in synaptic plasticity and intellectual development.
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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.