Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo(a)pyrene
Open accessAbstract
The focus of this study was to characterize the impact of gestational exposure to benzo(a)pyrene [B(a)P] on modulation of glutamate receptor subunit expression that is critical for the maintenance of synaptic plasticity mechanisms during hippocampal or cortical development in offspring. Previous studies have demonstrated that hippocampal and/or cortical synaptic plasticity (as measured by long-term potentiation and S1-cortex spontaneous/evoked neuronal activity) and learning behavior (as measured by fixed-ratio performance operant testing) is significantly impaired in polycyclic aromatic or halogenated aromatic hydrocarbon-exposed offspring as compared to controls. These previous studies have also revealed that brain to body weight ratios are greater in exposed offspring relative to controls indicative of intrauterine growth retardation which has been shown to manifest as low birth weight in offspring. Recent epidemiological studies have identified an effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children [Perera FP, Rauh V, Whyatt RM, Tsai WY, Tang D, Diaz D, et al. Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children. Environ Health Perspect 2006;114:1287-92]. The present study utilizes a well-characterized animal model to test the hypothesis that gestational exposure to B(a)P causes dysre…
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PAHs converge on related mechanisms through AhR activation; BaP reduces glutamate concentration and glutamate receptor expression, thereby weakening hippocampal LTP and impairing learning and memory; anthracene disrupts cholinergic signaling through acetylcholinesterase inhibition, leading to prolonged presence of acetylcholine in the synaptic cleft.
“PAHs converge on related mechanisms through AhR activation; BaP, for example, reduces glutamate concentration and glutamate receptor expression, thereby weakening hippocampal LTP and impairing learning and memory, while anthracene further disrupts cholinergic signaling through acetylcholinesterase inhibition which leads to the prolonged presence of acetylcholine in the synaptic cleft (Brown et al.”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Brown et al., 2007
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Translating developmental time across mammalian species
Clancy, B., Darlington, R. B., & Finlay, B. L. (2001) · Neuroscience · doi:10.1016/s0306-4522(01)00171-3 · Cited by 1,221 · see citing works
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Self-citationJocsak, G., Kiss, D. S., Alymbaeva, D., Diebald, A., Zsarnovszky, A., Heinzlmann, A., & Bartha, T. (2026) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2026.1821381 · Cited by 1 · see citing works
- Authors
- Brown, L. A., Khousbouei, H., Goodwin, J. S., Irvin-Wilson, C. V., Ramesh, A., Sheng, L., McCallister, M. M., Jiang, G. C. T., Aschner, M., & Hood, D. B.
- Affiliations
- Meharry Medical College (US)
- Vanderbilt University (US)
- Corresponding author
- Hood, Darryl B.
- Venue
- NeuroToxicology
- Publisher
- Elsevier BV
- Published
- 2007-09
- Volume
- 28
- Issue
- 5
- Pages
- 965-978
- ISSN
- 0161-813X (ISSN-L)
- PMC
- PMC2276633
- OpenAlex
- W2055506207
- Cited by
- 110
- References
- 1
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 7 · 2023: 3 · 2022: 2 · 2021: 5 · 2020: 7 · 2019: 6 · 2018: 4 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 8 · 2013: 8 · 2012: 10
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- NeuroToxicology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Vanderbilt University
- National Institutes of Health
- National Institute of Mental Health (T32MH065782)
- National Cancer Institute (U54CA091408, R03CA130112, R01CA142845)
- National Institute of General Medical Sciences (S06GM008037)
- National Institute of Neurological Disorders and Stroke (U54NS041071, U54NS41071-0002)
- National Institute of Environmental Health Sciences (S11ES014156, R15ES012168)
- National Center for Research Resources (G12 RR 03032-19, G12RR003032, U54RR019192)
- Division of Integrative Organismal Systems
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- benzo[a]pyrene, prenatal exposure, polycyclic aromatic hydrocarbons, ionotropic glutamate receptors, NMDA receptor subunits, AMPA receptor subunits, synaptic plasticity, hippocampus, prenatal neurodevelopment, developmental gene expression, long-term potentiation, fetal growth restriction, neurobehavioral deficits, learning behavior, primary neuronal cultures
- MeSH terms
- Animals, Benzo(a)pyrene, Brain, Cells, Cultured, Electrophysiology, Environmental Pollutants, Female, Immunohistochemistry, Learning Disabilities, Neuronal Plasticity, Neurons, Pregnancy, Prenatal Exposure Delayed Effects, RNA, Messenger, Down-Regulation, Receptors, N-Methyl-D-Aspartate, Receptors, Glutamate, Receptors, AMPA, Reverse Transcriptase Polymerase Chain Reaction, Rats
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