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

  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},
  volume={39 3},
Late Prenatal Immune Activation in Mice Leads to Behavioral and Neurochemical Abnormalities Relevant to the Negative Symptoms of Schizophrenia
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
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
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
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
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.


Maternal Influenza Infection Causes Marked Behavioral and Pharmacological Changes in the Offspring
It is found that respiratory infection of pregnant mice with the human influenza virus yields offspring that display highly abnormal behavioral responses as adults, as in schizophrenia and autism, and maternal injection of the synthetic double-stranded RNA polyinosinic-polycytidylic acid causes a PPI deficit in the offspring in the absence of virus.
Immune Activation During Pregnancy in Rats Leads to a PostPubertal Emergence of Disrupted Latent Inhibition, Dopaminergic Hyperfunction, and Altered Limbic Morphology in the Offspring: A Novel Neurodevelopmental Model of Schizophrenia
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.
Post-pubertal emergence of disrupted latent inhibition following prenatal immune activation
The hypothesis that immune activation during pregnancy may lead to long-term abnormalities mimicking those observed in schizophrenia is supported.
Schizophrenia: genetics and the maternal immune response to viral infection.
It is proposed that prenatal exposure to influenza induces maternal antibodies which then cross-react with proteins in the developing foetal brain, becomingfoetal autoantibodies, the biological substrate for a proportion of adult schizophrenia.
Infection and autoimmunity as etiologic factors in schizophrenia: a review and reappraisal.
  • D. Kirch
  • Medicine, Psychology
    Schizophrenia bulletin
  • 1993
No research evidence to date irrefutably indicates an infectious or autoimmune etiologic process in schizophrenia, and it is probably unreasonable, however, to view schizophrenia as having a single cause.
Immunopathology and Viral Reactivation: A General Theory of Schizophrenia
A theory is proposed that explains a broad range of clinical manifestations in schizophrenia by postulating defective alpha-interferon (alFN) regulation resulting in excessive effect is postulated to cause schizophrenia.
Schizophrenia and viral infection during neurodevelopment: a focus on mechanisms
  • B. Pearce
  • Psychology, Medicine
    Molecular Psychiatry
  • 2001
Consideration is given to a new hypothesis that some cases of schizophrenia could be instigated by a viral infection that disrupts developing inhibitory circuits, consequently unleashing glutamatergic neurotransmission leading to selective excitotoxicity, and a degenerative disease course.
Defective corticogenesis and reduction in Reelin immunoreactivity in cortex and hippocampus of prenatally infected neonatal mice
Prenatally-infected murine brains from postnatal day 0 showed significant reductions in reelin-positive cell counts in layer I of neocortex and other cortical and hippocampal layers when compared to controls and prenatal viral infection caused decreases in neocortical and hippocampusal thickness.
Borna disease virus-induced hippocampal dentate gyrus damage is associated with spatial learning and memory deficits