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Open AccessJournal ArticleDOI

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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Citations
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Journal ArticleDOI

Differential mGluR5 expression in response to the same stress causes individually adapted hippocampal network activity.

TL;DR: Data suggest a causal relationship between individual differences in the changes in hippocampal mGluR5 expression induced by repetitive restraint stress and the accompanying changes in ensemble neural activity in the hippocampus.
Journal ArticleDOI

Prenatal stress effects on offspring brain and behavior: Mediators, alterations and dysregulated epigenetic mechanisms.

TL;DR: Different brain alterations induced by prenatal stress such as in neural pruning processes, neural circuit formation, brain structural connectivity and epigenetic systems regulating neural gene expression are under focus in the second part of the review.
Dissertation

Animal Models of Prophylaxis and Prevention of Schizophrenia: Prenatal Seasonal Influenza Vaccine and Postnatal Valproate

TL;DR: The data suggest that further work is needed to make firm conclusions about the behavioural effects of the influenza vaccine, and an analysis of valproate treatment on cortical neuron morphology in Disc1 L100P mice, a model for schizophrenia.
Journal ArticleDOI

The Role of MeCP2 in Regulating Synaptic Plasticity in the Context of Stress and Depression

TL;DR: It is concluded that MeCP2 is a promising target for the development of novel, more efficacious therapeutics for the treatment of stress-related disorders such as depression.
Book ChapterDOI

Environmental epigenetics of sex differences in the brain.

TL;DR: This chapter addresses epigenetics in the context of sex differences, discussing the intersection between genetics and gonadal hormones and their effect in the brain at discrete developmental periods.
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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