A stereological comparison of GAD67 and reelin expression in the hippocampal stratum oriens of offspring from two mouse models of maternal inflammation during pregnancy

Harvey, Louise; Boksa, Patricia

doi:10.1016/j.neuropharm.2011.11.022

Cited by 83 publications

(82 citation statements)

References 73 publications

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“…Deficiencies of reelin expression could also be responsible for a large range of neurodevelopmental issues (17), and the heterozygous (Reel +/− ) mouse (30), exhibiting a permanent disruption of reelin expression, is considered to be a model of schizophrenia. Previous studies reported that early or mid-gestation prenatal challenges with poly I:C or LPS induced a deficit in Rln + hippocampal neurons in young rodents, most particularly in the stratum oriens of CA1 and the dentate gyrus (31)(32)(33). In the present study, we found an early (P10) deficit in reelin-expressing neurons after prenatal LPS, most prominent in the CA3 area.…”

Section: Prenatal Lps Effects On Reelin Neuronssupporting

confidence: 69%

N-acetyl-cysteine prevents pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge in rats

et al. 2013

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Background: Prenatal infection is a major risk factor for the occurrence of neuropsychiatric disorders. These have been associated with hippocampal neuroanatomical and functional abnormalities. In the present study, we evaluated the occurrence of pyramidal cell disarray and reelin neuronal deficit in the hippocampus, and the protective role of N-acetyl-cysteine (NAC) in a rodent experimental model of prenatal immune challenge. Methods: Sprague-Dawley rats received either 500 μg/kg of endotoxin (lipopolysaccharide, LPS) or 2 ml/kg of isotonic saline by i.p. injection on day 19 of gestation. After LPS injection, rats were or were not maintained on a preventive treatment of NAC (5 g/l in tap water), up to delivery. The pyramidal cell orientation and the number and type of reelin-expressing neurons were determined in male offspring. results: Prenatal LPS challenge led to permanent pyramidal cell disarray and to an early and transient decreased density of reelin-immunoreactive neurons. These disorders, more pronounced in the CA3 area, were prevented by NAC. conclusion: Hippocampal cytoarchitectural alterations and reelin deficiency may be involved in the development of remote cognitive impairments in this model. The antioxidant NAC is an efficient neuroprotective drug that underlines the role of oxidative stress in prenatal infection and associated neurodevelopmental damage.

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Section: Prenatal Lps Effects On Reelin Neuronssupporting

confidence: 69%

N-acetyl-cysteine prevents pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge in rats

et al. 2013

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“…Indeed, immune-related prenatal adversities have been repeatedly linked with a higher risk of neurodevelopmental psychiatric disorders, including schizophrenia, autism, and bipolar disorder (Brown and Derkits 2010;Patterson 2011;Marangoni et al 2016). These epidemiological associations are further supported by translational work in animal models demonstrating abnormal brain development and behavioral dysfunctions following prenatal administration of infectious pathogens or immune activating agents (Meyer and Feldon 2010;Harvey and Boksa 2012;Meyer 2014).…”

Section: Introductionmentioning

confidence: 95%

“…The model is based on maternal administration of the viral mimetic poly(I:C) (=polyriboinosinic-polyribocytidilic acid), which induces a cytokine-associated viral-like acute phase response in maternal and fetal compartments, including the fetal brain (Meyer et al 2009). Prenatal poly(I:C) treatment in rodents has repeatedly been shown to cause multiple behavioral and cognitive disturbances in the offspring, many of which are implicated in developmental psychiatric disorders such as schizophrenia and autism (Meyer et al 2009;Meyer and Feldon 2010;Harvey and Boksa 2012;Meyer 2014). The poly(I:C) administration model thus offers a unique opportunity to explore genome-wide transcriptomic changes following prenatal exposure to an etiologically relevant risk factor, and to further link such changes with neurobehavioral and MRI-detectable abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Genome-Wide Transcriptional Profiling and Structural Magnetic Resonance Imaging in the Maternal Immune Activation Model of Neurodevelopmental Disorders

et al. 2016

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Prenatal exposure to maternal infection increases the risk of neurodevelopmental disorders, including schizophrenia and autism. The molecular processes underlying this pathological association, however, are only partially understood. Here, we combined unbiased genome-wide transcriptional profiling with follow-up epigenetic analyses and structural magnetic resonance imaging to explore convergent molecular and neuromorphological alterations in corticostriatal areas of adult offspring exposed to prenatal immune activation. Genome-wide transcriptional profiling revealed that prenatal immune activation caused a differential expression of 116 and 251 genes in the medial prefrontal cortex and nucleus accumbens, respectively. A large part of genes that were commonly affected in both brain areas were related to myelin functionality and stability. Subsequent epigenetic analyses indicated that altered DNA methylation of promoter regions might contribute to the differential expression of myelin-related genes. Quantitative relaxometry comparing T 1 , T 2 , and myelin water fraction revealed sparse increases in T 1 relaxation times and consistent reductions in T 2 relaxation times. Together, our multisystem approach demonstrates that prenatal viral-like immune activation causes myelin-related transcriptional and epigenetic changes in corticostriatal areas. Even though these abnormalities do not seem to be associated with overt white © The Author 2017. Published by Oxford University Press. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.Downloaded from https://academic.oup.com/cercor/article-abstract/27/6/3397/2333950 by University of Zurich user on 23 November 2017 matter reduction, they may provide a molecular mechanism whereby prenatal infection can impair myelin functionality and stability.

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“…The nature and/or severity of these changes are influenced by various factors, most notably the identity and/or intensity of the pathogen (51,94), the gestational timing of exposure (97), and the genetic background of the infected host (2,96,154). Despite this, it seems that maternal exposure to distinct infectious or immune system-activating agents leads to partially overlapping immune responses in the fetal system.…”

Section: Peripheral (And Central) Inflammationmentioning

confidence: 99%

Long-term pathological consequences of prenatal infection: beyond brain disorders

Labouesse

Langhans

Meyer

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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A stereological comparison of GAD67 and reelin expression in the hippocampal stratum oriens of offspring from two mouse models of maternal inflammation during pregnancy

Cited by 83 publications

References 73 publications

N-acetyl-cysteine prevents pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge in rats

N-acetyl-cysteine prevents pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge in rats

Genome-Wide Transcriptional Profiling and Structural Magnetic Resonance Imaging in the Maternal Immune Activation Model of Neurodevelopmental Disorders

Long-term pathological consequences of prenatal infection: beyond brain disorders

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