Late prenatal immune activation in mice leads to behavioral and neurochemical abnormalities relevant to the negative symptoms of schizophrenia
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Based on the human epidemiological association between prenatal infection and higher risk of schizophrenia, a number of animal models have been established to explore the long-term brain and behavioral consequences of prenatal immune challenge. Accumulating evidence suggests that the vulnerability to specific forms of schizophrenia-related abnormalities is critically influenced by the precise timing of the prenatal immunological insult. In the present study, we tested the hypothesis whether late prenatal immune challenge in mice may induce long-term behavioral and neurochemical dysfunctions primarily associated with the negative symptoms of schizophrenia. We found that prenatal exposure to the viral mimic polyriboinosinic-polyribocytidilic acid (Poly-I:C; 5 mg/kg, i.v.) on gestation day (GD) 17 led to significant deficits in social interaction, anhedonic behavior, and alterations in the locomotor and stereotyped behavioral responses to acute apomorphine (APO) treatment in both male and female offspring. In addition, male but not female offspring born to immune challenged mothers displayed behavioral/cognitive inflexibility as indexed by the presence of an abnormally enhanced latent inhibition (LI) effect. Prenatal immune activation in late gestation also led to numerous, partly sex-specific changes in basal neurotransmitter levels, including reduced dopamine (DA) and glutamate contents in the prefrontal cortex and hippocampus, as well as reduced γ-aminobutyric acid (GABA) and glycine contents in the hippocampus and prefrontal cortex, respectively. The constellation of behavioral and neurochemical abnormalities emerging after late prenatal Poly-I:C exposure in mice leads us to conclude that this immune-based experimental model provides a powerful neurodevelopmental animal model especially for (but not limited to) the negative symptoms of schizophrenia.
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Prenatal exposure to polyinosinic:polycytidilic acid is a robust experimental model with well-characterized pathological and behavioral changes relevant to schizophrenia.
“In this regard, prenatal exposure to the immunostimulant polyinosinic:polycytidilic acid has been shown to represent a robust experimental model with a well-characterized evolution of pathologic and behavioural changes relevant to schizophrenia (Bitanihirwe et al., 2010; Giovanoli et al., 2013; Nyffeler et al., 2006; Richetto et al., 2013; Vuillermot et al., 2010)(Meyer, 2013).”
From Perineuronal nets and schizophrenia: The importance of neuronal coatings (2014) · cites this paper as Bitanihirwe et al., 2010
Animal models of systemic prenatal infection induce deficits in social behavior in offspring.
“deficits in social behavior (Bitanihirwe et al., 2010; Machado et al., 2015; Malkova et al., 2012; Smith et al., 2007)”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Bitanihirwe et al., 2010
Prenatal high-dose poly(I:C) in mice caused abnormalities in attentional shifting in adult males but not females.
“The first study noted abnormalities in attentional shifting in adult male, but not female, mice treated prenatally with a high dose of poly(I:C) (Bitanihirwe et al., 2010).”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Bitanihirwe et al., 2010
Animal models of systemic prenatal infection induce decreased cognitive flexibility in offspring.
“decreased cognitive flexibility (Bitanihirwe et al., 2010)”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Bitanihirwe et al., 2010
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- Authors
- Bitanihirwe, B. K., Peleg-Raibstein, D., Mouttet, F., Feldon, J., & Meyer, U.
- Affiliations
- ETH Zurich (CH)
- Corresponding author
- Meyer, Urs
- Venue
- Neuropsychopharmacology
- Published
- 2010-08-25
- Volume
- 35
- Issue
- 12
- Pages
- 2462-2478
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3055332
- OpenAlex
- W2024028366
- Cited by
- 237
- References
- 95
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 11 · 2023: 10 · 2022: 17 · 2021: 13 · 2020: 11 · 2019: 15 · 2018: 18 · 2017: 12 · 2016: 22 · 2015: 22 · 2014: 23 · 2013: 18 · 2012: 15
- FWCI
- 5.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation
- National Alliance for Research on Schizophrenia and Depression
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (116719, 100309, 3100A0)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- prenatal immune activation, schizophrenia, negative symptoms, poly(I:C), viral mimic, late pregnancy, social interaction deficits, anhedonia, latent inhibition, cognitive inflexibility, sex differences, dopamine, glutamate, GABA, glycine, neurotransmitter levels, prefrontal cortex, hippocampus
- MeSH terms
- Animals, Behavior, Animal, Disease Models, Animal, Dopamine, Female, gamma-Aminobutyric Acid, Glycine, Hippocampus, Male, Mice, Inbred C57BL, Poly I-C, Pregnancy, Prenatal Exposure Delayed Effects, Schizophrenia, Schizophrenic Psychology, Sex Characteristics, Prefrontal Cortex, Glutamic Acid, Central Nervous System Viral Diseases, Mice
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