Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.


The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Glutamatergic neurons in rodent models respond to nanoscale particulate urban air pollutants in vivo and in vitro.

Authors: Morgan, Todd E; Davis, David A; Iwata, Nahoko; Tanner, Jeremy A; Snyder, David; Ning, Zhi; Kam, Winnie; Hsu, Yu-Tien; Winkler, Jeremy W; Chen, Jiu-Chiuan; Petasis, Nicos A; Baudry, Michel; Sioutas, Constantinos; Finch, Caleb E

Published In Environ Health Perspect, (2011 Jul)

Abstract: Inhalation of airborne particulate matter (PM) derived from urban traffic is associated with pathology in the arteries, heart, and lung; effects on brain are also indicated but are less documented.We evaluated rodent brain responses to urban nanoscale (< 200 nm) PM (nPM).Ambient nPM collected near an urban freeway was transferred to aqueous suspension and reaerosolized for 10-week inhalation exposure of mice or directly applied to rat brain cell cultures.Free radicals were detected by electron paramagnetic resonance in the nPM 30 days after initial collection. Chronic inhalation of reaerosolized nPM altered selected neuronal and glial activities in mice. The neuronal glutamate receptor subunit (GluA1) was decreased in hippocampus, whereas glia were activated and inflammatory cytokines were induced [interleukin-1ýý (IL-1ýý), tumor necrosis factor-ýý (TNFýý)] in cerebral cortex. Two in vitro models showed effects of nPM suspensions within 24-48 hr of exposure that involved glutamatergic functions. In hippocampal slice cultures, nPM increased the neurotoxicity of NMDA (N-methyl-d-aspartic acid), a glutamatergic agonist, which was in turn blocked by the NMDA antagonist AP5 [(2R)-amino-5-phosphonopentanoate]. In embryonic neuron cultures, nPM impaired neurite outgrowth, also blocked by AP5. Induction of IL-1ýý and TNFýý in mixed glia cultures required higher nPM concentrations than did neuronal effects. Because conditioned media from nPM-exposed glia also impaired outgrowth of embryonic neurites, nPM can act indirectly, as well as directly, on neurons in vitro.nPM can affect embryonic and adult neurons through glutamatergic mechanisms. The interactions of nPM with glutamatergic neuronal functions suggest that cerebral ischemia, which involves glutamatergic excitotoxicity, could be exacerbated by nPM.

PubMed ID: 21724521 Exiting the NIEHS site

MeSH Terms: 2-Amino-5-phosphonovalerate/pharmacology; Animals; Brain Ischemia/etiology; Cells, Cultured; Cerebral Cortex/drug effects; Glutamic Acid/drug effects; Hippocampus/drug effects*; Hippocampus/immunology; Inhalation Exposure/analysis; Interleukin-1alpha/genetics; Interleukin-1alpha/immunology; Interleukin-1alpha/metabolism; Male; Mice; Mice, Inbred C57BL; N-Methylaspartate/antagonists & inhibitors; N-Methylaspartate/toxicity; Neuroglia/drug effects*; Neuroglia/immunology; Neurons/drug effects*; Particulate Matter/chemistry; Particulate Matter/toxicity*; RNA, Messenger/genetics; RNA, Messenger/metabolism; Rats; Receptors, AMPA/agonists; Tumor Necrosis Factor-alpha/genetics; Tumor Necrosis Factor-alpha/immunology; Tumor Necrosis Factor-alpha/metabolism; Vehicle Emissions/toxicity*

to Top