ArticleJournal of neurochemistry2013
Urban air pollutants reduce synaptic function of CA1 neurons via an NMDA/NȮ pathway in vitro.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Air pollution: a latent key driving force of dementia.BMC public health · 2024Pooled it
- Ambient air pollution and neurotoxicity on brain structure: Evidence from women's health initiative memory study.Annals of neurology · 2015Trial
- Prenatal exposure to particulate matter impairs offspring behavior via hippocampal NMDA receptor reduction: an in vivo and ex vivo study.Environment international · 2026Article
- Air pollution decreases postsynaptic PSD-95 and NMDA receptor subunits in synaptosomes from mouse cerebral cortex.Environmental pollution (Barking, Essex : 1987) · 2025Article
- Long-Term Exposure to Traffic-Related Air Pollution and Noise and Dynamic Brain Connectivity across Adolescence.Environmental health perspectives · 2025Article
- Emerging Stroke Risk Factors: A Focus on Infectious and Environmental Determinants.Journal of cardiovascular development and disease · 2024Review
- Air Pollution-Related Neurotoxicity Across the Life Span.Annual review of pharmacology and toxicology · 2023Review
- Mechanistic considerations and biomarkers level in nickel-induced neurodegenerative diseases: An updated systematic review.IBRO neuroscience reports · 2022Review
- Air Pollution and Headache Disorders.Annals of Indian Academy of Neurology · 2022Article
- The pathogenic effects of particulate matter on neurodegeneration: a review.Journal of biomedical science · 2022Review
- A mechanistic view on the neurotoxic effects of air pollution on central nervous system: risk for autism and neurodegenerative diseases.Environmental science and pollution research international · 2021Review
- The Air We Breathe: Air Pollution as a Prevalent Proinflammatory Stimulus Contributing to Neurodegeneration.Frontiers in cellular neuroscience · 2021Article
- Long-Term Ambient Air Pollution Exposures and Brain Imaging Markers in Korean Adults: The Environmental Pollution-Induced Neurological EFfects (EPINEF) Study.Environmental health perspectives · 2020Article
- Traffic-related air pollutants (TRAP-PM) promote neuronal amyloidogenesis through oxidative damage to lipid rafts.Free radical biology & medicine · 2020Article
- Particulate matter and episodic memory decline mediated by early neuroanatomic biomarkers of Alzheimer's disease.Brain : a journal of neurology · 2020Article
- The Effects of Air Pollution on the Brain: a Review of Studies Interfacing Environmental Epidemiology and Neuroimaging.Current environmental health reports · 2018Review
- Oxidative Potential of Ambient Particulate Matter in Beirut during Saharan and Arabian Dust Events.Atmospheric environment (Oxford, England : 1994) · 2018Article
- The emerging risk of exposure to air pollution on cognitive decline and Alzheimer's disease - Evidence from epidemiological and animal studies.Biomedical journal · 2018Review
- A critical review of assays for hazardous components of air pollution.Free radical biology & medicine · 2018Review
- The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade.Journal of Alzheimer's disease : JAD · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Airborne particulate matter (PM) from urban vehicular aerosols altered glutamate receptor functions and induced glial inflammatory responses in rodent models after chronic exposure. Potential neurotoxic mechanisms were analyzed in vitro. In hippocampal slices, 2 h exposure to aqueous nanosized PM (nPM) selectively altered post-synaptic proteins in cornu ammonis area 1 (CA1) neurons: increased GluA1, GluN2A, and GluN2B, but not GluA2, GluN1, or mGlur5; increased post synaptic density 95 and spinophilin, but not synaptophysin, while dentate gyrus (DG) neurons were unresponsive. In hippocampal slices and neurons, MitoSOX red fluorescence was increased by nPM, implying free radical production. Specifically, NȮ production by slices was increased within 15 min of exposure to nPM with dose dependence, 1-10 μg/mL. Correspondingly, CA1 neurons exhibited increased nitrosylation of the GluN2A receptor and dephosphorylation of GluN2B (S1303) and of GluA1 (S831 & S845). Again, DG neurons were unresponsive to nPM. The induction of NȮ and nitrosylation were inhibited by AP5, an NMDA receptor antagonist, which also protects neurite outgrowth in vitro from inhibition by nPM. Membrane injury (EthidiumD-1 uptake) showed parallel specificity. Finally, nPM decreased evoked excitatory post-synaptic currents of CA1 neurons. These findings further document the selective impact of nPM on glutamatergic functions and identify novel responses of NMDA receptor-stimulated NȮ production and nitrosylation reactions during nPM-mediated neurotoxicity. We present three new findings of rapid hippocampal slice responses to nPM (nano-sized particulate matter from urban traffic): increased NȮ production within 15 min; nitrosylation of glutamatergic NMDA receptors; and, reduced excitatory postsynaptic currents in CA1 neurons. AP5 (NMDA receptor antagonist) blocked nPM-mediated NȮ and receptor nitrosylation. Ca(2+) influx is a likely mechanism.
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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.