Prenatal Immune Activation Interacts with Genetic Nurr1 Deficiency in the Development of Attentional Impairments
Open accessAbstract
Prenatal exposure to infection has been linked to increased risk of neurodevelopmental brain disorders, and recent evidence implicates altered dopaminergic development in this association. However, since the relative risk size of prenatal infection appears relatively small with respect to long-term neuropsychiatric outcomes, it is likely that this prenatal insult interacts with other factors in shaping the risk of postnatal brain dysfunctions. In the present study, we show that the neuropathological consequences of prenatal viral-like immune activation are exacerbated in offspring with genetic predisposition to dopaminergic abnormalities induced by mutations in Nurr1, a transcription factor highly essential for normal dopaminergic development. We combined a mouse model of heterozygous genetic deletion of Nurr1 with a model of prenatal immune challenge by the viral mimetic poly(I:C) (polyriboinosinic polyribocytidilic acid). In our gene-environment interaction model, we demonstrate that the combination of the genetic and environmental factors not only exerts additive effects on locomotor hyperactivity and sensorimotor gating deficits, but further produces synergistic effects in the development of impaired attentional shifting and sustained attention. We further demonstrate that the combination of the two factors is necessary to trigger maldevelopment of prefrontal cortical and ventral striatal dopamine systems. Our findings provide evidence for specific gene-environment interactions in the emergence of enduring attentional impairments and neuronal abnormalities pertinent to dopamine-associated brain disorders such as schizophrenia and attention deficit/hyperactivity disorder, and further emphasize a critical role of abnormal dopaminergic development in these etiopathological processes.
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Animal models of systemic prenatal infection induce difficulty in sustained attention in offspring.
“difficulty in sustained attention (Vuillermot et al., 2012)”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Vuillermot et al., 2012
Prenatal immune activation combined with genetic Nurr1 deficiency in adult male mice caused impairments in sustained attention and attentional shifting.
“This study noted impairments in both sustained attention (using the two-choice discrimination test) and attentional shifting in adult male mice that were exposed to prenatal immune activation and had genetic Nurr1 deficiency (Vuillermot et al., 2012).”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Vuillermot et al., 2012
Prenatal poly(I:C) exposure impaired working memory in a matching-to-position dry maze paradigm.
“prenatal poly(I:C) exposure impaired working memory in a matching-to-position paradigm in the dry maze (Vuillermot et al., 2012)”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Vuillermot et al., 2012
Prenatal immune activation and Nurr1 deficiency had additive effects on spontaneous locomotor hyperactivity in open field.
“prenatal immune activation and Nurr1 deficiency exerted additive effects on spontaneous locomotor hyperactivity in the open field test (Vuillermot et al., 2012).”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Vuillermot et al., 2012
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- Authors
- Vuillermot, S., Joodmardi, E., Perlmann, T., Ove Ögren, S., Feldon, J., & Meyer, U.
- Affiliations
- ETH Zurich (CH)
- Ludwig Cancer Research (BE)
- Corresponding author
- Meyer, Urs
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2012-01-11
- Volume
- 32
- Issue
- 2
- Pages
- 436-451
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6621065
- OpenAlex
- W2161703304
- Cited by
- 127
- References
- 70
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 12 · 2021: 10 · 2020: 6 · 2019: 6 · 2018: 8 · 2017: 5 · 2016: 8 · 2015: 18 · 2014: 13 · 2013: 14 · 2012: 10
- FWCI
- 7.25
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by-nc-sa)
- ETH Zürich Research Collection
- Funders
- National Science Foundation
- National Alliance for Research on Schizophrenia and Depression
- European Commission (FP7/2007, 259679)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (116719, 100309)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- prenatal immune activation, Nurr1, gene-environment interaction, attention deficits, poly(I:C), viral infection, sensorimotor gating, locomotor hyperactivity, prefrontal cortex, ventral striatum, schizophrenia, attention deficit hyperactivity disorder, neurodevelopmental disorders
- MeSH terms
- Animals, Attention Deficit Disorder with Hyperactivity, Disease Models, Animal, Female, Male, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Schizophrenia, Virus Diseases, Mice, Knockout, Neurocognitive Disorders, Genetic Predisposition to Disease, Autoimmune Diseases of the Nervous System, Mice, Nuclear Receptor Subfamily 4, Group A, Member 2, Mice, 129 Strain
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