Maternal immune activation leads to behavioral and pharmacological changes in the adult offspring.

@article{Zuckerman2005MaternalIA,
  title={Maternal immune activation leads to behavioral and pharmacological changes in the adult offspring.},
  author={Lee Zuckerman and Ina Weiner},
  journal={Journal of psychiatric research},
  year={2005},
  volume={39 3},
  pages={
          311-23
        }
}
Late Prenatal Immune Activation in Mice Leads to Behavioral and Neurochemical Abnormalities Relevant to the Negative Symptoms of Schizophrenia
TLDR
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.
Aberrant neural synchrony in the maternal immune activation model: using translatable measures to explore targeted interventions
TLDR
The ability of the MIA intervention to model neurodevelopmental aspects of schizophrenia pathology provides a useful platform from which to investigate the ontogeny of aberrant synchronous processes and the way in which the model expresses translatable deficits such as aberrant synchronization and reduced PPI will allow researchers to explore novel intervention strategies targeted to these changes.
Prenatal and postnatal maternal contributions in the infection model of schizophrenia
TLDR
The adoption of prenatally immune-challenged neonates by control surrogate mothers does not possess any protective effects against the subsequent emergence of psychopathology in adulthood, and the present study highlights for the first time that the adoption of prenatal control animals by immune- Challenged rearing mothers is sufficient to precipitate learning disabilities in the juvenile and adult offspring.
Maternal immune activation produces neonatal excitability defects in offspring hippocampal neurons from pregnant rats treated with poly I:C
TLDR
C cultured pyramidal-like hippocampal neurons prepared from neonatal (P0-P2) offspring of pregnant rats injected with poly I:C exhibited significantly lower intrinsic excitability and stronger spike frequency adaptation, compared to saline, suggesting that MIA-induced alterations could occur earlier at neonatal/early postnatal stages.
The role of cytokines in mediating effects of prenatal infection on the fetus: implications for schizophrenia
TLDR
Data suggest that effects of maternal LPS exposure on the developing fetal brain are not mediated by the direct action of LPS, but via indirect actions at the level of the maternal circulation or placenta.
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Prenatal immune activation induced by peripheral administration of the synthetic cytokine releaser polyriboinosinic–polyribocytidilic acid to pregnant dams may provide a neurodevelopmental model of schizophrenia that reproduces a putative inducing factor; mimics the temporal course as well as some central abnormalities of the disorder; and predicts responsiveness to antipsychotic drugs.
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