Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase. - Wikidata - wikimedia - TriplyDB

Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase.

Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase.

http://www.wikidata.org/entity/Q34722527

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Glutathione precursor N-acetyl-cysteine modulates EEG synchronization in schizophrenia patients: a double-blind, randomized, placebo-controlled trial GABAergic interneuron origin of schizophrenia pathophysiology.GABAB-mediated rescue of altered excitatory-inhibitory balance, gamma synchrony and behavioral deficits following constitutive NMDAR-hypofunction.GABA neurons and the mechanisms of network oscillations: implications for understanding cortical dysfunction in schizophrenia Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia Glutamatergic deficits and parvalbumin-containing inhibitory neurons in the prefrontal cortex in schizophrenia A New Perspective on Delusional States - Evidence for Claustrum Involvement.Insights into cortical oscillations arising from optogenetic studies The cytokine model of schizophrenia: emerging therapeutic strategies Selenoproteins in nervous system development and function The role of glutamatergic inputs onto parvalbumin-positive interneurons: relevance for schizophrenia Glutamate Decarboxylase 67 Deficiency in a Subset of GABAergic Neurons Induces Schizophrenia-Related Phenotypes Global quantitative analysis of phosphorylation underlying phencyclidine signaling and sensorimotor gating in the prefrontal cortex.IL-6 mediated degeneration of forebrain GABAergic interneurons and cognitive impairment in aged mice through activation of neuronal NADPH oxidase Schizophrenia: One Coat of Many Colors Drug models of schizophrenia Common mechanisms of excitatory and inhibitory imbalance in schizophrenia and autism spectrum disorders Impaired selenoprotein expression in brain triggers striatal neuronal loss leading to co-ordination defects in mice.Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration Deletion of selenoprotein M leads to obesity without cognitive deficits Dysfunctional GABAergic inhibition in the prefrontal cortex leading to "psychotic" hyperactivation Schizophrenia.Sepsis-induced selective parvalbumin interneuron phenotype loss and cognitive impairments may be mediated by NADPH oxidase 2 activation in mice.Spatial and temporal boundaries of NMDA receptor hypofunction leading to schizophrenia.GluN2D N-Methyl-d-Aspartate Receptor Subunit Contribution to the Stimulation of Brain Activity and Gamma Oscillations by Ketamine: Implications for Schizophrenia Targeting Oxidative Stress and Aberrant Critical Period Plasticity in the Developmental Trajectory to Schizophrenia.Competition between the Brain and Testes under Selenium-Compromised Conditions: Insight into Sex Differences in Selenium Metabolism and Risk of Neurodevelopmental Disease Glutamatergic synaptic dysregulation in schizophrenia: therapeutic implications.Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia Cannabidiol attenuates sensorimotor gating disruption and molecular changes induced by chronic antagonism of NMDA receptors in mice.Parvalbumin and GAD65 interneuron inhibition in the ventral hippocampus induces distinct behavioral deficits relevant to schizophrenia.Dysregulation of the axonal trafficking of nuclear-encoded mitochondrial mRNA alters neuronal mitochondrial activity and mouse behavior The effect of deficient muscarinic signaling on commonly reported biochemical effects in schizophrenia and convergence with genetic susceptibility loci in explaining symptom dimensions of psychosis.Electrophysiological and behavioral responses to ketamine in mice with reduced Akt1 expression.Social isolation exacerbates schizophrenia-like phenotypes via oxidative stress in cortical interneurons How Nox2-containing NADPH oxidase affects cortical circuits in the NMDA receptor antagonist model of schizophrenia.Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.Is lead exposure in early life an environmental risk factor for Schizophrenia? Neurobiological connections and testable hypotheses.Inhibitory interneurons, oxidative stress, and schizophrenia.Contribution of NMDA receptor hypofunction in prefrontal and cortical excitatory neurons to schizophrenia-like phenotypes.

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P2860

Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase.

http://www.wikidata.org/entity/Q34722527

description

2007 nî lūn-bûn

@nan

2007 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2007 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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name

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

@ast

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

@en

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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type

label

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

@ast

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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prefLabel

Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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Ketamine-induced loss of pheno ...... is mediated by NADPH-oxidase.

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Diep N Dao

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Grigoriy Shekhtman

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Jacinta Lucero

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Kevin L Quick

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Laura L Dugan

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M Margarita Behrens

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Sameh S Ali

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10.1126/SCIENCE.1148045

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2007-12-01T00:00:00Z

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