Altered expression of pro-inflammatory and developmental genes in the fetal brain in a mouse model of maternal infection

Liverman, Christopher S.; Kaftan, Harold A; Cui, Lisa; Hersperger, Stephen G.; Taboada, Eugenio; Klein, Robert M.; Berman, Nancy E.J.

doi:10.1016/j.neulet.2006.01.064

Cited by 71 publications

(48 citation statements)

References 54 publications

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“…Indeed, a decreased expression of transcription factors regulating neuronal migration was observed 4 h after LPS injection to pregnant dams, supporting the hypothesis of a migration disorder (28). On the other hand, prenatal immune challenge may also alter neurogenesis in the fetal and young offspring's brain (29).…”

Section: Discussionsupporting

confidence: 57%

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: Discussionsupporting

confidence: 57%

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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“…Treatment of mouse dams with lipopolysaccharide (LPS), which also elevates levels of proinflammatory cytokines, leads to increased expression of Necdin (Ndn) in the offspring, with upregulation persisting up to 12 h following LPS exposure. 249 As previously noted, NDN is located on the chromosomal region 15q11-13 associated with PWS. These findings indicate that prenatal exposure to inflammatory agents in mice may provide a model for aberrant gene expression relevant to early abnormal development in autism.…”

Section: Mouse Models Of Environmental Contributions To Autism Etiologymentioning

confidence: 79%

Advances in behavioral genetics: mouse models of autism

2007

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Autism is a neurodevelopmental syndrome with markedly high heritability. The diagnostic indicators of autism are core behavioral symptoms, rather than definitive neuropathological markers. Etiology is thought to involve complex, multigenic interactions and possible environmental contributions. In this review, we focus on genetic pathways with multiple members represented in autism candidate gene lists. Many of these pathways can also be impinged upon by environmental risk factors associated with the disorder. The mouse model system provides a method to experimentally manipulate candidate genes for autism susceptibility, and to use environmental challenges to drive aberrant gene expression and cell pathology early in development. Mouse models for fragile X syndrome, Rett syndrome and other disorders associated with autistic-like behavior have elucidated neuropathology that might underlie the autism phenotype, including abnormalities in synaptic plasticity. Mouse models have also been used to investigate the effects of alterations in signaling pathways on neuronal migration, neurotransmission and brain anatomy, relevant to findings in autistic populations. Advances have included the evaluation of mouse models with behavioral assays designed to reflect disease symptoms, including impaired social interaction, communication deficits and repetitive behaviors, and the symptom onset during the neonatal period. Research focusing on the effect of gene-by-gene interactions or genetic susceptibility to detrimental environmental challenges may further understanding of the complex etiology for autism.

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“…Proinflammatory cytokines are regarded as a connecting link between intrauterine infection during pregnancy and subsequent disturbances of brain functions in the fetus. Injection of LPS to pregnant mice induces increased expression of TNF , IL-1 , and MCP-1 in fetuses (Liverman et al, 2006). In rats, the expression of TNF is observed as early as 1 h after LPS injection and its level remaining unchanged for 24 h, while the level of IL-1 gradually decreases.…”

Section: Neuroendocrine and Immune Regulatory Mechanisms In The Develmentioning

confidence: 96%

“…This assumption is confirmed by recent data on the effect of LPS on fetal brain development. It has been shown that LPS induces the synthesis of the vascular endothelial growth factor, nerve growth factor (NGF), antiapoptotic protein YB-1, neuronal differentiation factor (necdin), and BDNF in the fetal rat brain cortex (Liverman et al, 2006). On day 18 of embryonic development in mice, LPS suppresses the expression of factors involved in neuron migration and axonal cone growth, namely, of semaphorin 5b and chromatin-associated Groucho protein (Liverman et al, 2006).…”

Section: Neuroendocrine and Immune Regulatory Mechanisms In The Develmentioning

confidence: 99%

“…It has been shown that LPS induces the synthesis of the vascular endothelial growth factor, nerve growth factor (NGF), antiapoptotic protein YB-1, neuronal differentiation factor (necdin), and BDNF in the fetal rat brain cortex (Liverman et al, 2006). On day 18 of embryonic development in mice, LPS suppresses the expression of factors involved in neuron migration and axonal cone growth, namely, of semaphorin 5b and chromatin-associated Groucho protein (Liverman et al, 2006). In addition, LPS increases the content of glial fibrillary acidic protein (GFAP), an intermediate filament protein, in hippocampal and cortical astrocytes and reduces the content of myelin and immunoreactivity of the microglia in the offspring of LPS-injected rats during postnatal development.…”

Section: Neuroendocrine and Immune Regulatory Mechanisms In The Develmentioning

confidence: 99%

See 1 more Smart Citation

Interactions Between Reproductive and Immune Systems During Ontogeny: Roles of GnRH, Sex Steroids, and Immunomediators

Захарова¹,

Izvolskaia²

2012

Sex Steroids

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Altered expression of pro-inflammatory and developmental genes in the fetal brain in a mouse model of maternal infection

Cited by 71 publications

References 54 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

Advances in behavioral genetics: mouse models of autism

Interactions Between Reproductive and Immune Systems During Ontogeny: Roles of GnRH, Sex Steroids, and Immunomediators

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