The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Maternal poly I:C exposure during pregnancy regulates TNFα, BDNF, and NGF expression in neonatal brain and the maternal–fetal unit of the rat
Abstract
Maternal infection during pregnancy is associated with increased risk for neurodevelopmental disorders. Polyriboinosinic-polyribocytidilic acid (poly I:C) or saline was administered to rats to model maternal infection; levels of TNFalpha, brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF) were determined by ELISA. TNFalpha was significantly increased in maternal plasma, placenta, and amniotic fluid, while it was significantly decreased in fetal liver/spleen and neonatal brain. NGF and BDNF were significantly decreased in the placenta and fetal liver/spleen. There was no change in BDNF or NGF in the fetal or neonatal brain. Changes in TNFalpha, BDNF, and NGF after maternal exposure to poly I:C represent a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders.
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“Some of the strongest support for maternal infection as a contributor to autism has come from the maternal immune activation (MIA) model, which has repeatedly shown consistent results, helping to establish a subset of autism that is supported by observations of autism-relevant atypical behaviors.”
From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Gilmore et al, 2005
In the citing paper
“The MIA model in its most common design involves challenging pregnant rodents via direct infection (eg, influenza, Escherichia coli) or the dsRNA mimic poly (I:C); significant immunological, neurodevelopmental, and behavioral changes are then observed in the offspring”
From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Gilmore et al, 2005
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Metadata
- Authors
- Gilmore, J. H., Jarskog, L. F., & Vadlamudi, S.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Gilmore, John H.
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2005-02
- Volume
- 159
- Issue
- 1-2
- Pages
- 106-112
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W1989871271
- Cited by
- 177
- References
- 40
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 7 · 2022: 6 · 2021: 5 · 2020: 12 · 2019: 5 · 2018: 12 · 2017: 8 · 2016: 3 · 2015: 15 · 2014: 8 · 2013: 8 · 2012: 16
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH-60352, R01MH060352)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Keywords
- maternal infection, poly(I:C), pregnancy, TNF-α, brain-derived neurotrophic factor, nerve growth factor, neurotrophins, neonatal brain, placenta, amniotic fluid, neurodevelopmental disorders, neuroinflammation
- MeSH terms
- Amniotic Fluid, Animals, Animals, Newborn, Brain, Female, Injections, Intraperitoneal, Liver, Maternal-Fetal Exchange, Poly I-C, Pregnancy, Pregnancy Proteins, Prenatal Exposure Delayed Effects, Spleen, Tumor Necrosis Factor-alpha, Down-Regulation, Up-Regulation, Rats, Sprague-Dawley, Maternal Exposure, Brain-Derived Neurotrophic Factor, Nerve Growth Factor, Rats
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