Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala

O’Loughlin, Elaine; Pakan, Janelle M.P.; Yilmazer-Hanke, Deniz; McDermott, Kieran W.

doi:10.1186/s12974-017-0981-8

Cited by 99 publications

(68 citation statements)

References 42 publications

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“…Prenatal infection is one of the suspected causes of schizophrenia and it can make astrocytes hypersensitive to stimuli in the future, which may cause an enhanced response in the central nervous system (Takahashi and Sakurai, 2013). Maternal immune activation on day 12 of mice embryonic development leads to changes in astrocytes and microglia and increases the GFAP levels, which indicate astrogliosis in the amygdala (O'Loughlin et al, 2017), but in another study, mice prenatal immune activation did not change astrocyte density (Giovanoli et al, 2016). Activation of astrocytes during rat embryonic development can disrupt the cortical and thalamocortical formation (Beamer et al, 2017).…”

Section: Prenatal Infection and Mother Deprivation Lead To Schizophreniamentioning

confidence: 99%

Alterations of Astrocytes in the Context of Schizophrenic Dementia

et al. 2020

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The levels of the astrocyte markers (GFAP, S100B) were increased unevenly in patients with schizophrenia. Reactive astrogliosis was found in approximately 70% of patients with schizophrenia. The astrocytes play a major role in etiology and pathogenesis of schizophrenia. Astrocytes produce the components that altered in schizophrenia extracellular matrix system which are involved in inflammation, functioning of interneurons, glio-, and neurotransmitter system, especially glutamate system. Astrocytes activate the interneurons through glutamate release and ATP. Decreased expression of astrocyte glutamate transporters was observed in patients with schizophrenia. Astrocytes influence on N-methyl-d-aspartate (NMDA) receptors via Dserine, an agonist of the glycine-binding site of NMDA receptors, and kynurenic acid, an endogenous antagonist. NMDA receptors, on its turn, control the impulses of dopamine neurons. Therefore following theories of schizophrenia are proposed. They are a) activation of astrocytes for neuroinflammation, b) glutamate and dopamine theory, as astrocyte products control the activity of NMDA receptors, which influence on the dopamine neurons.

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Section: Prenatal Infection and Mother Deprivation Lead To Schizophreniamentioning

confidence: 99%

Alterations of Astrocytes in the Context of Schizophrenic Dementia

et al. 2020

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“…Astrocytes and microglia are active participants in propagating and regulating neuroinflammation within the brain. 32,33 GFAP and Iba-1 are markers of astrocytes and microglia. 34 The levels of Iba-1 but not GFAP were enhanced in the amygdala after CFA injection, indicating the involvement of microglia in the peripheral pain process.…”

Section: Polydatin Attenuates Inflammatory Response In the Amygdalamentioning

confidence: 99%

Anxiolytic effects of polydatin through the blockade of neuroinflammation in a chronic pain mouse model

et al. 2020

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Background: Chronic pain is frequently comorbid with anxiety disorder, thereby complicating its treatment. Polydatin, a component from the root of Polygonum cuspidatum, has shown neuroprotection in the central nervous system. However, its effects on pain and anxiety processing have been rarely investigated. In this study, mice were injected with complete Freund's adjuvant (CFA) at the hindpaw to induce pain-and anxiety-like behaviors. Results: Treatment with polydatin (25 mg/kg) alleviated the anxiety-like behaviors but not pain perception in these mice. Polydatin treatment reversed the upregulation of N-methyl-D-aspartic acid receptors and GluA1-containing a-amino-3hydroxy-5-methyl-4-isoxazole-propionic acid receptors in the amygdala of CFA-injected mice. Additionally, this treatment reduced the levels of proinflammatory cytokines, namely, tumor necrosis factor-alpha and interleukin-1b, in the amygdala. Furthermore, activated nuclear factor kappa-B signaling was blocked in the amygdala from CFA-injected mice. By using docking technology, we found potential structural binding between polydatin and IjB kinase beta. Conclusion: This study indicates the anxiolytic effects of polydatin by suppressing inflammatory cytokines in the amygdala.

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“…Others also hypothesized that an increase of the solidity value occurs during the morphological shift from a ramified to an amoeboid shape upon neuroinflammatory insults, and represents a de-ramified or bushy morphology [94,95], a phenotype seen upon exposure to stress [96]. In a bacterial MIA mouse model, microglia were previously shown to shift their morphology to an ameboid shape in adolescent (P40) offspring amygdala [97]. Although the microglial morphological changes we observed varied between layers, similarly they could indicate a general shift from a surveillant-ramified state to an amoeboid shape.…”

Section: Discussionmentioning

confidence: 99%

Microglial and peripheral immune priming is partially sexually dimorphic in adolescent mouse offspring exposed to maternal high-fat diet

Bordeleau

Lacabanne

Cossío

et al. 2020

Preprint

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Background Maternal nutrition is critical for proper fetal development. While increased nutrient intake is essential during pregnancy, an excessive consumption of certain nutrients, like fat, can lead to long-lasting detrimental consequences on the offspring. Animal work investigating the consequences of maternal high-fat diet (mHFD) revealed in the offspring a maternal immune activation (MIA) phenotype associated with increased inflammatory signals. This inflammation was proposed as one of the mechanisms causing neuronal circuit dysfunction, notably in the hippocampus, by altering the brain-resident macrophages –microglia. However, the understanding of mechanisms linking inflammation and microglial activities to pathological brain development remains limited. We hypothesized that mHFD-induced inflammation could prime microglia by altering their specific gene expression signature, population density and/or functions. Methods We used an integrative approach combining molecular techniques, confocal and scanning electron microscopy, to investigate the effects of mHFD vs control diet on inflammatory priming, as well as microglial density, distribution, morphology, and ultrastructure in mice. These analyses were performed on the mothers, and/or their adolescent offspring at postnatal day (P) 30. Results Our study revealed that mHFD results in MIA defined by increased circulating levels of interleukin (IL)-6 in the mothers. This phenotype was associated with an exacerbated inflammatory response to peripheral lipopolysaccharide in mHFD-exposed offspring of both sexes. Microglial morphology was also altered and there were increased microglial interactions with astrocytes in the hippocampus CA1 of mHFD-exposed male offspring, as well as decreased microglia-associated extracellular space pockets in the same region of mHFD-exposed offspring of the two sexes. A decreased mRNA expression of the inflammatory-regulating cytokine Tgfb1 and microglial receptors Tmem119, Trem2 and Cx3cr1 was additionally measured in the hippocampus of mHFD-exposed offspring, especially in males. Conclusions Here, we described how dietary habits during pregnancy and nurturing, particularly the consumption of an enriched fat diet, can influence peripheral immune priming in the offspring. We also found that microglia are affected in terms of gene expression signature, morphology and interactions with the hippocampal parenchyma, in a partially sexually dimorphic manner, which may contribute to the adverse neurodevelopmental outcomes on the offspring.

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Acute in utero exposure to lipopolysaccharide induces inflammation in the pre- and postnatal brain and alters the glial cytoarchitecture in the developing amygdala

Cited by 99 publications

References 42 publications

Alterations of Astrocytes in the Context of Schizophrenic Dementia

Alterations of Astrocytes in the Context of Schizophrenic Dementia

Anxiolytic effects of polydatin through the blockade of neuroinflammation in a chronic pain mouse model

Microglial and peripheral immune priming is partially sexually dimorphic in adolescent mouse offspring exposed to maternal high-fat diet

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