Behaviour and hippocampus-specific changes in spiny mouse neonates after treatment of the mother with the viral-mimetic poly I:C at mid-pregnancy
Abstract
Epidemiological studies have suggested a link between prenatal exposure to bacterial or viral infections and subsequent development of mental disorders such as schizophrenia and autism. Animal models to study the prenatal origin of such outcomes of pregnancy have largely used conventional rodents which are immature at birth compared to the human neonate, and doses of the infective agent (i.e., lipopolysaccharide, Poly I:C) have been large enough to cause sickness behaviour in the mother. In this study we have used the spiny mouse (Acomys cahirinus) whose offspring have completed organogenesis at birth, and a single subcutaneous injection of a low (0.5mg/kg) dose of polyriboinosinic-polyribocytidilic acid (Poly I:C) at mid gestation (20 days, term is 39 days). The treatment had no effect on maternal, fetal or neonatal survival, or postnatal growth of the offspring. However, offspring showed significant impairments in non-spatial memory and learning tasks, and motor activity. Brain histology examined at 1 and 100 days of age revealed significant decreases in reelin, increased GFAP expression, and increased numbers of activated microglia, specifically in the hippocampus. This study provides evidence that a prenatal subclinical infection can have profound effects on brain development that are long-lasting.
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Mid-gestation injection of maternal mice with low-dose immunostimulatory poly I:C to mimic viral infection significantly impaired non-spatial memory, learning, and motor activity in the offspring at 3 and 9 weeks of age.
“Mid-gestation injection of maternal mice with low-dose immunostimulatory polyinosinic:polycytidylic acid (poly I:C) to mimic viral infection significantly impaired non-spatial memory, learning, and motor activity in the offspring at 3 and 9 weeks of age (396).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [396]
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- Authors
- Ratnayake, U., Quinn, T. A., Castillo-Melendez, M., Dickinson, H., & Walker, D. W.
- Affiliations
- Monash University (AU)
- Corresponding author
- Ratnayake, Udani
- Venue
- Brain Behavior and Immunity
- Publisher
- Elsevier BV
- Published
- 2012-11
- Volume
- 26
- Issue
- 8
- Pages
- 1288-1299
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W2075035357
- Cited by
- 75
- References
- 65
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 3 · 2023: 1 · 2022: 6 · 2021: 5 · 2020: 2 · 2019: 4 · 2018: 8 · 2017: 1 · 2016: 5 · 2015: 7 · 2014: 14 · 2013: 12
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- RMIT Research Repository (RMIT University Library) (submittedVersion)
- Figshare (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- prenatal infection, poly(I:C), spiny mouse, Acomys cahirinus, hippocampus, non-spatial memory, learning deficits, motor activity, reelin, glial fibrillary acidic protein, microglial activation, brain development, schizophrenia, autism spectrum disorder, maternal immune activation, neonatal behavior
- MeSH terms
- Reelin Protein, Animals, Animals, Newborn, Behavior, Animal, Disease Models, Animal, Female, Hippocampus, Mothers, Neuroglia, Poly I-C, Pregnancy, Prenatal Exposure Delayed Effects, Mice
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