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Induction of Maternal Immune Activation in Mice at Mid-gestation Stage with Viral Mimic PolyI:C
Published on: March 25, 2016
Developmental disruption of perineuronal nets in the medial prefrontal cortex after maternal immune activation
John W Paylor1,2, Brittney R Lins3, Quentin Greba3
1Neuroscience and Mental Health Institute, University of Alberta, Edmonton, T6G 2E1, AB, Canada.
Insights
Maternal immune activation (MIA) during pregnancy reduces perineuronal nets (PNNs) in the adult offspring's prefrontal cortex. This MIA-induced PNN deficit may underlie schizophrenia-like cognitive dysfunction.
Area of Science:
- Neuroscience
- Developmental Biology
- Psychiatry
Background:
- Maternal infection during pregnancy is a risk factor for schizophrenia in offspring.
- Maternal immune activation (MIA) animal models exhibit schizophrenia-like phenotypes.
- Schizophrenia is associated with prefrontal cortex (PFC) cognitive deficits and perineuronal net (PNN) abnormalities.
Purpose of the Study:
- To investigate the developmental impact of MIA on PNNs in the rat prefrontal cortex (PFC).
- To determine if MIA-induced PNN deficits are linked to parvalbumin-expressing cells.
- To explore region-specific PNN alterations following MIA.
Main Methods:
- Utilized a rat model of MIA induced by polyinosinic-polycytidylic acid (polyI:C) injection during pregnancy.
- Quantified PNNs and parvalbumin-positive cells in the PFC and amygdala of offspring across developmental stages.
- Assessed the proportion of parvalbumin cells ensheathed by PNNs.
Main Results:
- Selective reductions in PFC PNNs were observed in polyI:C offspring, emerging in early adulthood.
- No significant changes in parvalbumin cell density were found.
- A decreased percentage of parvalbumin cells were surrounded by PNNs in polyI:C offspring.
- Altered developmental expression of PNNs was noted in the amygdala.
Conclusions:
- MIA induces region-specific developmental abnormalities in PNNs within the offspring's PFC.
- The polyI:C rat model replicates key neuropathological features of schizophrenia.
- MIA-related PNN deficits may contribute to cognitive and emotional dysfunction in schizophrenia.
Abstract:
Maternal infection during pregnancy increases the risk of offspring developing schizophrenia later in life. Similarly, animal models of maternal immune activation (MIA) induce behavioural and anatomical disturbances consistent with a schizophrenia-like phenotype in offspring. Notably, cognitive impairments in tasks dependent on the prefrontal cortex (PFC) are observed in humans with schizophrenia and in offspring after MIA during pregnancy. Recent studies of post-mortem tissue from individuals with schizophrenia revealed deficits in extracellular matrix structures called perineuronal nets (PNNs), particularly in PFC. Given these findings, we examined PNNs over the course of development in a well-characterized rat model of MIA using polyinosinic-polycytidylic acid (polyI:C). We found selective reductions of PNNs in the PFC of polyI:C offspring which did not manifest until early adulthood. These deficits were not associated with changes in parvalbumin cell density, but a decrease in the percentage of parvalbumin cells surrounded by a PNN. Developmental expression of PNNs was also significantly altered in the amygdala of polyI:C offspring. Our results indicate MIA causes region specific developmental abnormalities in PNNs in the PFC of offspring. These findings confirm the polyI:C model replicates neuropathological alterations associated with schizophrenia and may identify novel mechanisms for cognitive and emotional dysfunction in the disorder.
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