Reduced cortical activity due to a shift in the balance between excitation and inhibition in a mouse model of Rett syndrome - Test2 - elhamkhani - TriplyDB

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

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

http://www.wikidata.org/entity/Q24530286

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Alterations of GABAergic signaling in autism spectrum disorders Autism and brain development Activity-dependent synaptogenesis: regulation by a CaM-kinase kinase/CaM-kinase I/betaPIX signaling complex.Mouse neurexin-1alpha deletion causes correlated electrophysiological and behavioral changes consistent with cognitive impairments.Pathophysiology of locus ceruleus neurons in a mouse model of Rett syndrome Emerging pharmacotherapies for neurodevelopmental disorders A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice Neurophysiological and computational principles of cortical rhythms in cognition Epigenetics in the mature mammalian brain: effects on behavior and synaptic transmission Regulatory long non-coding RNAs and neuronal disorders Balanced gene regulation by an embryonic brain ncRNA is critical for adult hippocampal GABA circuitry A direct role for FMRP in activity-dependent dendritic mRNA transport links filopodial-spine morphogenesis to fragile X syndrome.The common BDNF polymorphism may be a modifier of disease severity in Rett syndrome Signaling mechanisms linking neuronal activity to gene expression and plasticity of the nervous system Partial reversal of Rett Syndrome-like symptoms in MeCP2 mutant mice The odyssey of MeCP2 and parental imprinting Clinical and Neurobiological Relevance of Current Animal Models of Autism Spectrum Disorders.Recent advances in understanding synaptic abnormalities in Rett syndrome Developmental Dynamics of Rett Syndrome Rett Syndrome: Crossing the Threshold to Clinical Translation Characterizing autism spectrum disorders by key biochemical pathways.Genes, circuits, and precision therapies for autism and related neurodevelopmental disorders Excitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum Disorders Prenatal stress and inhibitory neuron systems: implications for neuropsychiatric disorders The impact of MeCP2 loss- or gain-of-function on synaptic plasticity The roles of PDGF in development and during neurogenesis in the normal and diseased nervous system BDNF deregulation in Rett syndrome GABAergic signaling as therapeutic target for autism spectrum disorders Changes in plasticity across the lifespan: cause of disease and target for intervention Role of mecp2 in experience-dependent epigenetic programming GABA and glutamate pathways are spatially and developmentally affected in the brain of Mecp2-deficient mice The Intense World Theory – A Unifying Theory of the Neurobiology of Autism Insulin-Like Growth Factor 1 and Related Compounds in the Treatment of Childhood-Onset Neurodevelopmental Disorders A Subset of Autism-Associated Genes Regulate the Structural Stability of Neurons.Prospective MEG biomarkers in ASD: pre-clinical evidence and clinical promise of electrophysiological signatures.Discovery of Rare Mutations in Autism: Elucidating Neurodevelopmental Mechanisms Rett syndrome: disruption of epigenetic control of postnatal neurological functions Circuit-specific intracortical hyperconnectivity in mice with deletion of the autism-associated Met receptor tyrosine kinase Use of transcranial magnetic stimulation in autism spectrum disorders Sleep and circadian dysfunction in neurodegenerative disorders: insights from a mouse model of Huntington's disease

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

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2005 nî lūn-bûn

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2005 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2005年の論文

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Reduced cortical activity due ...... a mouse model of Rett syndrome

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Reduced cortical activity due ...... a mouse model of Rett syndrome

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Arianna Maffei

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Gina G Turrigiano

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Qiang Chang

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Vardhan S Dani

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P2860

Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2

Expression of MeCP2 in postmitotic neurons rescues Rett syndrome in mice

Homeostatic plasticity in the developing nervous system

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

MECP2 is progressively expressed in post-migratory neurons and is involved in neuronal maturation rather than cell fate decisions

Cellular and network mechanisms of rhythmic recurrent activity in neocortex

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice

Mice with truncated MeCP2 recapitulate many Rett syndrome features and display hyperacetylation of histone H3

Rate, timing, and cooperativity jointly determine cortical synaptic plasticity.

Selective dendritic alterations in the cortex of Rett syndrome.

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