Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice. - Wikidata - awgldk - TriplyDB

Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice.

Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice.

http://www.wikidata.org/entity/Q42027886

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Frontal GABA levels change during working memory Nucleocytoplasmic shuttling of dysbindin-1, a schizophrenia-related protein, regulates synapsin I expression Synaptic plasticity, neural circuits, and the emerging role of altered short-term information processing in schizophrenia.Clinical and molecular genetics of psychotic depression Gene × Environment Interactions in Schizophrenia: Evidence from Genetic Mouse Models Dysbindin promotes the post-endocytic sorting of G protein-coupled receptors to lysosomes Animal Models of Psychosis: Current State and Future Directions.Behavioral characterization of mice overexpressing human dysbindin-1.Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways.Dysbindin-1 mutant mice implicate reduced fast-phasic inhibition as a final common disease mechanism in schizophrenia.Beyond the dopamine receptor: novel therapeutic targets for treating schizophrenia.Dysbindin-containing complexes and their proposed functions in brain: from zero to (too) many in a decade.Cognitive control deficits in schizophrenia: mechanisms and meaning Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.The use of the puzzle box as a means of assessing the efficacy of environmental enrichment.Mutations in the BLOC-1 subunits dysbindin and muted generate divergent and dosage-dependent phenotypes.Genetic modifiers of abnormal organelle biogenesis in a Drosophila model of BLOC-1 deficiency.Synaptic dysbindin-1 reductions in schizophrenia occur in an isoform-specific manner indicating their subsynaptic location.Neurofibromin regulates corticostriatal inhibitory networks during working memory performance Avoiding mouse traps in schizophrenia genetics: lessons and promises from current and emerging mouse models.Working memory impairment in calcineurin knock-out mice is associated with alterations in synaptic vesicle cycling and disruption of high-frequency synaptic and network activity in prefrontal cortex Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance.Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia.Dysbindin and Schizophrenia: it's dopamine and glutamate all over again.Dysbindin-1 genotype effects on emotional working memory MeCP2 regulates the synaptic expression of a Dysbindin-BLOC-1 network component in mouse brain and human induced pluripotent stem cell-derived neurons.An N-methyl-D-aspartate receptor agonist facilitates sleep-independent synaptic plasticity associated with working memory capacity enhancement The N-ethylmaleimide-sensitive factor and dysbindin interact to modulate synaptic plasticity.Fetal radiofrequency radiation exposure from 800-1900 mhz-rated cellular telephones affects neurodevelopment and behavior in mice Neurodevelopmental role for VGLUT2 in pyramidal neuron plasticity, dendritic refinement, and in spatial learning.Calcineurin Aγ is a Functional Phosphatase That Modulates Synaptic Vesicle Endocytosis Loss of dysbindin-1 in mice impairs reward-based operant learning by increasing impulsive and compulsive behavior Epistatic interaction between COMT and DTNBP1 modulates prefrontal function in mice and in humans Modeling neurodevelopmental cognitive deficits in tasks with cross-species translational validity The Proteome of BLOC-1 Genetic Defects Identifies the Arp2/3 Actin Polymerization Complex to Function Downstream of the Schizophrenia Susceptibility Factor Dysbindin at the Synapse Dysbindin Deficiency Modifies the Expression of GABA Neuron and Ion Permeation Transcripts in the Developing Hippocampus.Alterations of the myristoylated, alanine-rich C kinase substrate (MARCKS) in prefrontal cortex in schizophrenia Genetic influence on the working memory circuitry: behavior, structure, function and extensions to illness.Losing your inhibition: linking cortical GABAergic interneurons to schizophrenia.Electrophysiological endophenotypes in rodent models of schizophrenia and psychosis.

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P2860

Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice.

http://www.wikidata.org/entity/Q42027886

description

2009 nî lūn-bûn

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name

Dysbindin modulates prefrontal ...... rking memory function in mice.

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Dysbindin modulates prefrontal ...... rking memory function in mice.

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Dysbindin modulates prefrontal ...... rking memory function in mice.

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Neuropsychopharmacology

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Dysbindin modulates prefrontal ...... orking memory function in mice

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Antonieta Lavin

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Corey Jairl

http://www.w3.org/2001/XMLSchema#string

Heather Trantham-Davidson

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Matthew Tinsley

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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)

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

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

Impaired long-term memory retention and working memory in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia

Cellular basis of working memory

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

Neurobehavioral abnormalities in the dysbindin-1 mutant, sandy, on a C57BL/6J genetic background.

Ensemble codes involving hippocampal neurons are at risk during delayed performance tests.

Prefrontal neurons and the genetics of schizophrenia.

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10.1038/NPP.2009.90

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12

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34

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J. David Jentsch

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26704241

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1043847899

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19641486

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2762021

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