ArticleMolecular neurobiology2016
Lead Exposure Impairs Hippocampus Related Learning and Memory by Altering Synaptic Plasticity and Morphology During Juvenile Period.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Systemic review of genetic and epigenetic factors underlying differential toxicity to environmental lead (Pb) exposure.Environmental science and pollution research international · 2022Pooled it
- Chronic Lead Exposure and Tauopathies: Molecular Mechanisms of Neurotoxicity and Emerging Nanotherapeutic Strategies.Journal of toxicology · 2026Review
- Mixed exposure to lead, methylmercury, and cadmium aggravates spatial memory deficits via dopamine signaling pathways in the mouse hippocampus.Frontiers in public health · 2026Article
- Eucalyptol Attenuates Lead-Induced Anxiety-like Behaviors by Suppressing Oxidative Stress and Neuroinflammation, Modulating SIRT1/NF-κB Signaling, and Upregulating BDNF Expression.Biological trace element research · 2025Article
- Environmentally relevant lead exposure impacts gene expression in SH-SY5Y cells throughout neuronal differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Developmental Pb exposure increases rate of forgetting on a delayed matching-to-sample task among Mexican children.Science advances · 2025Article
- Glutamate-Mediated Neural Alterations in Lead Exposure: Mechanisms, Pathways, and Phenotypes.Toxics · 2025Review
- Chronic PbbioRxiv : the preprint server for biology · 2025Article
- Article
- Mitofilin-mtDNA Axis Mediates Chronic Lead Exposure-Induced Synaptic Plasticity Impairment of Hippocampal and Cognitive Deficits.Biomolecules · 2025Article
- Urinary Metal Levels, Cognitive Test Performance, and Dementia in the Multi-Ethnic Study of Atherosclerosis.JAMA network open · 2024Article
- Role of SIRT1 in Potentially Toxic Trace Elements (Lead, Fluoride, Aluminum and Cadmium) Associated Neurodevelopmental Toxicity.Biological trace element research · 2024Review
- Metal Toxicity and Dementia Including Frontotemporal Dementia: Current State of Knowledge.Antioxidants (Basel, Switzerland) · 2024Review
- Metals on the Menu-Analyzing the Presence, Importance, and Consequences.Foods (Basel, Switzerland) · 2024Review
- Single-cell investigation of lead toxicity from neurodevelopment to neurodegeneration: Current review and future opportunities.Current opinion in toxicology · 2024Article
- An Industry-Relevant Metal Mixture, Iron Status, and Reported Attention-Related Behaviors in Italian Adolescents.Environmental health perspectives · 2024Article
- Prenatal Metal Exposures and Child Social Responsiveness Scale Scores in 2 Prospective Studies.Environmental health insights · 2024Article
- Hippocampal LIMK1-mediated Structural Synaptic Plasticity in Neurobehavioral Deficits Induced by a Low-dose Heavy Metal Mixture.Molecular neurobiology · 2023Article
- Recent insights into autophagy and metals/nanoparticles exposure.Toxicological research · 2023Review
- Associations of an industry-relevant metal mixture with verbal learning and memory in Italian adolescents: The modifying role of iron status.Environmental research · 2023Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lead (Pb) is an environmental neurotoxic metal. Pb exposure may cause neurobehavioral changes, such as learning and memory impairment, and adolescence violence among children. Previous animal models have largely focused on the effects of Pb exposure during early development (from gestation to lactation period) on neurobehavior. In this study, we exposed Sprague-Dawley rats during the juvenile stage (from juvenile period to adult period). We investigated the synaptic function and structural changes and the relationship of these changes to neurobehavioral deficits in adult rats. Our results showed that juvenile Pb exposure caused fear-conditioned memory impairment and anxiety-like behavior, but locomotion and pain behavior were indistinguishable from the controls. Electrophysiological studies showed that long-term potentiation induction was affected in Pb-exposed rats, and this was probably due to excitatory synaptic transmission impairment in Pb-exposed rats. We found that NMDA and AMPA receptor-mediated current was inhibited, whereas the GABA synaptic transmission was normal in Pb-exposed rats. NR2A and phosphorylated GluR1 expression decreased. Moreover, morphological studies showed that density of dendritic spines declined by about 20 % in the Pb-treated group. The spine showed an immature form in Pb-exposed rats, as indicated by spine size measurements. However, the length and arborization of dendrites were unchanged. Our results suggested that juvenile Pb exposure in rats is associated with alterations in the glutamate receptor, which caused synaptic functional and morphological changes in hippocampal CA1 pyramidal neurons, thereby leading to behavioral changes.
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