Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures. - Test2 - elhamkhani - TriplyDB

Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.

Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.

http://www.wikidata.org/entity/Q37578480

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Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders Molecular underpinnings of prefrontal cortex development in rodents provide insights into the etiology of neurodevelopmental disorders Targeted pharmacological treatment of autism spectrum disorders: fragile X and Rett syndromes Rett syndrome: disruption of epigenetic control of postnatal neurological functions Loss of MeCP2 in cholinergic neurons causes part of RTT-like phenotypes via α7 receptor in hippocampus Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes Manipulations of MeCP2 in glutamatergic neurons highlight their contributions to Rett and other neurological disorders Characterization of Rett Syndrome-like phenotypes in Mecp2-knockout rats Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.What you seize is what you get: do we yet understand epilepsy in rett syndrome?Excitation/inhibition imbalance and impaired synaptic inhibition in hippocampal area CA3 of Mecp2 knockout mice Autism spectrum disorder and epilepsy: Disorders with a shared biology.Methyl CpG Binding Protein 2 Gene Disruption Augments Tonic Currents of γ-Aminobutyric Acid Receptors in Locus Coeruleus Neurons: IMPACT ON NEURONAL EXCITABILITY AND BREATHING.Longitudinal course of epilepsy in Rett syndrome and related disorders.Cell-Specific Regulation of N-Methyl-D-Aspartate Receptor Maturation by Mecp2 in Cortical Circuits.Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders.Pathway-driven discovery of epilepsy genes.Acute and crucial requirement for MeCP2 function upon transition from early to late adult stages of brain maturation Effects of early-life exposure to THIP on phenotype development in a mouse model of Rett syndrome.Enrichment of mutations in chromatin regulators in people with Rett syndrome lacking mutations in MECP2.Jointly reduced inhibition and excitation underlies circuit-wide changes in cortical processing in Rett syndrome.MeCP2 co-ordinates liver lipid metabolism with the NCoR1/HDAC3 corepressor complex.Effects of early-life exposure to THIP on brainstem neuronal excitability in the Mecp2-null mouse model of Rett syndrome before and after drug withdrawal.Whole Genome Expression Analysis in a Mouse Model of Tauopathy Identifies MECP2 as a Possible Regulator of Tau Pathology.Genetic disorders associated with postnatal microcephaly.Rett syndrome: a complex disorder with simple roots.Single-Gene Determinants of Epilepsy Comorbidity.Rescue of impaired sociability and anxiety-like behavior in adult cacna1c-deficient mice by pharmacologically targeting eIF2α.Neurophysiology and Regulation of the Balance Between Excitation and Inhibition in Neocortical Circuits.Haploinsufficiency of MeCP2-interacting transcriptional co-repressor SIN3A causes mild intellectual disability by affecting the development of cortical integrity.BDNF rescues prefrontal dysfunction elicited by pyramidal neuron-specific DTNBP1 deletion in vivo.Defects During Mecp2 Null Embryonic Cortex Development Precede the Onset of Overt Neurological Symptoms.Models and detection of spontaneous recurrent seizures in laboratory rodents.Association of Tag SNPs and Rare CNVs of the MIR155HG/miR-155 Gene with Epilepsy in the Chinese Han Population.Structural and functional differences in the barrel cortex of Mecp2 null mice.Epigenetics and Epilepsy.Rescue of hyperexcitability in hippocampal CA1 neurons from Mecp2 (-/y) mouse through surface potential neutralization.Loss of Causes Atypical Synaptic and Molecular Plasticity of Parvalbumin-Expressing Interneurons Reflecting Rett Syndrome-Like Sensorimotor Defects

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Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.

http://www.wikidata.org/entity/Q37578480

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on February 2014

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

@en

Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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JNEUROSCI.4900-12.2014

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Journal of Neuroscience

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Loss of MeCP2 from forebrain e ...... hyperexcitation and seizures.

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Barbara Beyer

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Matthew Peterson

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Wayne N Frankel

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Wen Zhang

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Zhong-wei Zhang

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P2860

Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett syndrome

Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome

Emotional processing in anterior cingulate and medial prefrontal cortex

MeCP2, a key contributor to neurological disease, activates and represses transcription

The story of Rett syndrome: from clinic to neurobiology

A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome

Learning and memory and synaptic plasticity are impaired in a mouse model of Rett syndrome

MeCP2 controls excitatory synaptic strength by regulating glutamatergic synapse number

Hippocampal synaptic plasticity is impaired in the Mecp2-null mouse model of Rett syndrome

Dysregulation of brain-derived neurotrophic factor expression and neurosecretory function in Mecp2 null mice

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2754-2763

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scholarly article

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10.1523/JNEUROSCI.4900-12.2014

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7

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2014-02-01T00:00:00Z

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3921436

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