Maternal immune activation during pregnancy increases limbic GABAA receptor immunoreactivity in the adult offspring: Implications for schizophrenia
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 i...
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| Published in | Neuroscience Vol. 143; no. 1; pp. 51 - 62 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Elsevier
17.11.2006
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0306-4522 |
| DOI | 10.1016/j.neuroscience.2006.07.029 |
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| 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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| AbstractList | 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. 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.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. |
| Author | Nyffeler, M. Knuesel, I. Yee, B.K. Feldon, J. Meyer, U. |
| Author_xml | – sequence: 1 givenname: M. surname: Nyffeler fullname: Nyffeler, M. – sequence: 2 givenname: U. surname: Meyer fullname: Meyer, U. – sequence: 3 givenname: B.K. surname: Yee fullname: Yee, B.K. – sequence: 4 givenname: J. surname: Feldon fullname: Feldon, J. – sequence: 5 givenname: I. surname: Knuesel fullname: Knuesel, I. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18305923$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17045750$$D View this record in MEDLINE/PubMed |
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| Keywords | Amygdala Central nervous system Schizophrenia Basal ganglion Encephalon Polyl:C Psychosis Pregnancy Prenatal Dentate gyrus neurodevelopment Gabaergic receptor A Hippocampus |
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| SubjectTerms | Adult and adolescent clinical studies Analysis of Variance Animals Behavior, Animal - drug effects Biological and medical sciences Cell Count - methods Cell Size - drug effects Disease Models, Animal Female Glial Fibrillary Acidic Protein - metabolism Immunohistochemistry - methods Limbic System - drug effects Limbic System - metabolism Limbic System - pathology Male Medical sciences Mice Mice, Inbred C57BL Poly I-C Pregnancy Prenatal Exposure Delayed Effects - immunology Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Receptors, GABA-A - metabolism Schizophrenia Schizophrenia - chemically induced Schizophrenia - metabolism Schizophrenia - pathology Statistics as Topic |
| Title | Maternal immune activation during pregnancy increases limbic GABAA receptor immunoreactivity in the adult offspring: Implications for schizophrenia |
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