Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia. - Test2 - elhamkhani - TriplyDB

Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia.

Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia.

http://www.wikidata.org/entity/Q30468313

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Synapse-specific contributions in the cortical pathology of schizophrenia High-frequency oscillations and the neurobiology of schizophrenia Impact of ketamine on neuronal network dynamics: translational modeling of schizophrenia-relevant deficits.Cytosolic Accumulation of L-Proline Disrupts GABA-Ergic Transmission through GAD Blockade Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia.How Nox2-containing NADPH oxidase affects cortical circuits in the NMDA receptor antagonist model of schizophrenia.Modeling psychiatric disorders at the cellular and network levels Mice with reduced NMDA receptor expression: more consistent with autism than schizophrenia?Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits.Interneuron precursor transplants in adult hippocampus reverse psychosis-relevant features in a mouse model of hippocampal disinhibition.Mutations in the BLOC-1 subunits dysbindin and muted generate divergent and dosage-dependent phenotypes.Automatic auditory processing deficits in schizophrenia and clinical high-risk patients: forecasting psychosis risk with mismatch negativity.Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia.The NMDA Receptor and Schizophrenia: From Pathophysiology to Treatment.Measuring the maturity of the fast-spiking interneuron transcriptional program in autism, schizophrenia, and bipolar disorder Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A "central hub" in schizophrenia pathophysiology?The NMDA receptor 'glycine modulatory site' in schizophrenia: D-serine, glycine, and beyond.Brain rhythms connect impaired inhibition to altered cognition in schizophrenia.Gene dosage in the dysbindin schizophrenia susceptibility network differentially affect synaptic function and plasticity Path from schizophrenia genomics to biology: gene regulation and perturbation in neurons derived from induced pluripotent stem cells and genome editing.MeCP2+/- mouse model of RTT reproduces auditory phenotypes associated with Rett syndrome and replicate select EEG endophenotypes of autism spectrum disorder.Mouse model of OPRM1 (A118G) polymorphism has altered hippocampal function.Ceftriaxone reverses ketamine-induced lasting EEG and astrocyte alterations in juvenile mice.A Role for the Transcription Factor Nk2 Homeobox 1 in Schizophrenia: Convergent Evidence from Animal and Human Studies Effects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus.Increased dysbindin-1B isoform expression in schizophrenia and its propensity in aggresome formation.Implicit Timing as the Missing Link between Neurobiological and Self Disorders in Schizophrenia?Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia.Sensory encoding in Neuregulin 1 mutants Selective loss of parvalbumin-positive GABAergic interneurons in the cerebral cortex of maternally stressed Gad1-heterozygous mouse offspring.Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus.Dynamical changes in neurological diseases and anesthesia.Losing your inhibition: linking cortical GABAergic interneurons to schizophrenia.Role of murine models in psychiatric illness drug discovery: a dimensional view.High-frequency neural oscillations and visual processing deficits in schizophrenia.Neural oscillations during non-rapid eye movement sleep as biomarkers of circuit dysfunction in schizophrenia.Convergence of circuit dysfunction in ASD: a common bridge between diverse genetic and environmental risk factors and common clinical electrophysiology.Electrophysiological endophenotypes in rodent models of schizophrenia and psychosis.Cellular and circuit models of increased resting-state network gamma activity in schizophrenia

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Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia.

http://www.wikidata.org/entity/Q30468313

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2011 nî lūn-bûn

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2011年の論文

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2011年論文

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Dysbindin-1 mutant mice implic ...... se mechanism in schizophrenia.

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Dysbindin-1 mutant mice implic ...... se mechanism in schizophrenia.

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Dysbindin-1 mutant mice implic ...... se mechanism in schizophrenia.

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Dysbindin-1 mutant mice implic ...... se mechanism in schizophrenia.

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Proceedings of the National Academy of Sciences of the United States of America

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Dysbindin-1 mutant mice implic ...... se mechanism in schizophrenia.

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Gregory C Carlson

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Hala A Kazi

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Konrad Talbot

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Laura Schlosser

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Quan H Phung

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P2860

Dysbindin-1 is a synaptic and microtubular protein that binds brain snapin

Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1)

Glutamatergic deficits and parvalbumin-containing inhibitory neurons in the prefrontal cortex in schizophrenia

Evidence of novel neuronal functions of dysbindin, a susceptibility gene for schizophrenia

Disrupted-in-Schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1

DTNBP1, a schizophrenia susceptibility gene, affects kinetics of transmitter release

Role of dysbindin in dopamine receptor trafficking and cortical GABA function

EEGLAB: an open source toolbox for analysis of single-trial EEG dynamics including independent component analysis

Cortical inhibitory neurons and schizophrenia

Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence

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