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Epigenetic modifications of GABAergic interneurons are associated with the schizophrenia-like phenotype induced by prenatal stress in mice.

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TLDR
Preliminary data show that prenatal stress in mice induces abnormalities in the DNA methylation network and in behaviors indicative of a schizophrenia-like phenotype, and PRS mice may be a valid model for the investigation of new drugs for schizophrenia treatment targetingDNA methylation.
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This article is published in Neuropharmacology.The article was published on 2013-05-01 and is currently open access. It has received 240 citations till now. The article focuses on the topics: Reelin & Prenatal stress.

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Intrauterine exposure to maternal stress alters Bdnf IV DNA methylation and telomere length in the brain of adult rat offspring.

TL;DR: Findings indicate a long‐term impact of prenatal stress on brain DNA methylation and telomere biology with relevance for behavioral and health outcomes, and contribute to a growing literature linking stress to intergenerational molecular changes.
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Schizophrenia and reelin: a model based on prenatal stress to study epigenetics, brain development and behavior

TL;DR: It is proposed that prenatal stress induces neurodevelopmental alterations in the prefrontal cortex that are expressed as cognitive impairment observed in schizophrenia and a unifying framework that links prenatal stress and prefrontal malfunction through epigenetic alterations of the reelin gene is proposed.
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Methyl CpG Binding Domain Ultra‐Sequencing: a novel method for identifying inter‐individual and cell‐type‐specific variation in DNA methylation

TL;DR: MBD Ultra‐Seq is a robust method for detecting DNA methylation in neurons derived from discrete brain regions of individual animals and is found that the neuronal methylome is characterized by greater CpG methylation as well as the enrichment of 5mC within intergenic loci.
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Examining the Reversibility of Long-Term Behavioral Disruptions in Progeny of Maternal SSRI Exposure

TL;DR: Findings indicate maternal FLX treatment, independent of maternal stress, can induce behavioral disruptions in mammalian offspring, thus contributing to the understanding of the developmental role of the serotonin system and the possible risks to offspring of SSRI treatment during pregnancy.
References
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Journal ArticleDOI

Cortical inhibitory neurons and schizophrenia

TL;DR: Convergent findings indicate that a deficiency in signalling through the TrkB neurotrophin receptor leads to reduced GABA synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia.
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The Developmental Origins of Adult Disease

TL;DR: It is shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth, and a new vision of optimal early human development is emerging which takes account of both short and long-term outcomes.
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Green fluorescent protein expression and colocalization with calretinin, parvalbumin, and somatostatin in the GAD67-GFP knock-in mouse.

TL;DR: A map of GFP distribution in the knock‐in mouse brain is constructed and many medium‐sized spherical somata emitting intense GFP fluorescence were observed in layer I, in accord with unidentified GFP‐positive cells.
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Decrease in reelin and glutamic acid decarboxylase67 (GAD67) expression in schizophrenia and bipolar disorder: A postmortem brain study

TL;DR: The selective down-regulation of RELN and GAD(67) in prefrontal cortex of patients with schizophrenia and bipolar disorder who have psychosis is consistent with the hypothesis that these parameters are vulnerability factors in psychosis; this plus the loss of the correlation between these 2 parameters that exists in nonpsychotic subjects support the hypotheses that these changes may be liability factors underlying psychosis.
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Dynamic DNA methylation programs persistent adverse effects of early-life stress

TL;DR: It is found that neuronal activity controlled the ability of MeCP2 to regulate activity-dependent transcription of the Avp gene and induced epigenetic marking, which can dynamically control DNA methylation in postmitotic neurons to generate stable changes in Avp expression that trigger neuroendocrine and behavioral alterations that are frequent features in depression.
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