Maternal immune activation during pregnancy increases limbic GABAA receptor immunoreactivity in the adult offspring: implications for schizophrenia
Abstract
Prenatal exposures to a variety of infections have been associated with an increased incidence of schizophrenia. We have reported that a single injection of the synthetic cytokine releaser PolyI:C to pregnant mice produced offspring that exhibited multiple schizophrenia-related behavioral deficits in adulthood. Here, we characterized the effect of maternal inflammation during fetal brain development on adult limbic morphology and expression of GABAA-receptors. The PolyI:C treatment did not induce morphological abnormalities but resulted in a significant increase in GABAA receptor subunit alpha2 immunoreactivity (IR) in the ventral dentate gyrus and basolateral amygdala in adult treated compared to control subjects. Correlative analyses between the a2 subunit IR in the ventral dentate gyrus and the performance in the prepulse inhibition paradigm revealed a significant correlation in controls that was however absent in the pathological condition. These results suggest that prenatal immune activation-induced disturbances of early brain development result in profound alterations in the limbic expression of GABAA receptors that may underlie the schizophrenia-related behavioral deficits in the adult mice.
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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 Nyffeler et al., 2006
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References 88 · Cited by 139
Research works printed but not linked: 1
- Roberts, 1972, Prospects for research on schizophrenia, Neurosci Res Program Bull, 10, 468
- Authors
- Nyffeler, M., Meyer, U., Yee, B. K., Feldon, J., & Knuesel, I.
- Affiliations
- ETH Zurich (CH)
- Corresponding author
- Knuesel, I.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2006-11
- Volume
- 143
- Issue
- 1
- Pages
- 51-62
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W1980320018
- Cited by
- 139
- References
- 88
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 4 · 2019: 8 · 2018: 3 · 2017: 3 · 2016: 7 · 2015: 14 · 2014: 13 · 2013: 9 · 2012: 11
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- maternal immune activation, prenatal infection, schizophrenia, limbic system, dentate gyrus, basolateral amygdala, prepulse inhibition, poly(I:C), prenatal inflammation, fetal brain development, schizophrenia risk
- MeSH terms
- Analysis of Variance, Animals, Behavior, Animal, Cell Count, Disease Models, Animal, Female, Glial Fibrillary Acidic Protein, Immunohistochemistry, Limbic System, Male, Mice, Inbred C57BL, Poly I-C, Pregnancy, Prenatal Exposure Delayed Effects, Receptors, GABA-A, Schizophrenia, Statistics as Topic, Cell Size, Mice
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