Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression. - Wikidata - awgldk - TriplyDB

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

http://www.wikidata.org/entity/Q37104018

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Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence Epigenetics of the depressed brain: role of histone acetylation and methylation A brief history of the development of antidepressant drugs: from monoamines to glutamate Altered functional protein networks in the prefrontal cortex and amygdala of victims of suicide Deletion of glutamate delta-1 receptor in mouse leads to aberrant emotional and social behaviors The E3 ligase APC/C-Cdh1 is required for associative fear memory and long-term potentiation in the amygdala of adult mice From synapse to nucleus: novel targets for treating depression.Elevated level of metabotropic glutamate receptor 2/3 in the prefrontal cortex in major depression.Reduced level of glutamic acid decarboxylase-67 kDa in the prefrontal cortex in major depression.Glutamatergic modulators: the future of treating mood disorders?Reduced metabotropic glutamate receptor 5 density in major depression determined by [(11)C]ABP688 PET and postmortem study.AAV-mediated overexpression of neuroserpin in the hippocampus decreases PSD-95 expression but does not affect hippocampal-dependent learning and memory.Lurasidone exerts antidepressant properties in the chronic mild stress model through the regulation of synaptic and neuroplastic mechanisms in the rat prefrontal cortex.Basolateral amygdala volume and cell numbers in major depressive disorder: a postmortem stereological study Novel glutamatergic agents for major depressive disorder and bipolar disorder.Glucocorticoid Induces Incoordination between Glutamatergic and GABAergic Neurons in the Amygdala.Incoordination among Subcellular Compartments Is Associated with Depression-Like Behavior Induced by Chronic Mild Stress Reduced levels of NR2A and NR2B subunits of NMDA receptor and PSD-95 in the prefrontal cortex in major depression Modulation of behavior by scaffolding proteins of the post-synaptic density.Targeting glutamatergic signaling for the development of novel therapeutics for mood disorders The Role of Neural Plasticity in Depression: From Hippocampus to Prefrontal Cortex Neuropathology of mood disorders: do we see the stigmata of inflammation?Increased PKC activity and altered GSK3β/NMDAR function drive behavior cycling in HINT1-deficient mice: bipolarity or opposing forces.Overview of glutamatergic neurotransmission in the nervous system.The Functional and Molecular Properties, Physiological Functions, and Pathophysiological Roles of GluN2A in the Central Nervous System.Targeting glutamate signalling in depression: progress and prospects.Treating the Synapse in Major Psychiatric Disorders: The Role of Postsynaptic Density Network in Dopamine-Glutamate Interplay and Psychopharmacologic Drugs Molecular Actions A complex interaction between glycine/NMDA receptors and serotonergic/noradrenergic antidepressants in the forced swim test in mice.Zinc transporters protein level in postmortem brain of depressed subjects and suicide victims.Attenuation of reserpine-induced pain/depression dyad by gentiopicroside through downregulation of GluN2B receptors in the amygdala of mice.Aberrant NMDA receptor DNA methylation detected by epigenome-wide analysis of hippocampus and prefrontal cortex in major depression.Excessive activation of the loop between the NR2B subunit of the N-methyl-d-aspartate receptor and glycogen synthase kinase-3β in the hippocampi of patients with major depressive disorder.Preclinical Models of Traumatic Brain Injury: Emerging Role of Glutamate in the Pathophysiology of Depression.

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Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

http://www.wikidata.org/entity/Q37104018

description

article científic

@ca

article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 23 June 2008

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@en

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@nl

type

label

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@en

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@nl

prefLabel

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@en

Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@nl

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S1461145708008985

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The International Journal of Neuropsychopharmacology

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Elevated levels of NR2A and PSD-95 in the lateral amygdala in depression.

@en

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Beata Karolewicz

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Craig A Stockmeier

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Dorota Maciag

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

Gregory A Ordway

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Katalin Szebeni

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Tempestt Gilmore

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P2860

Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein

Two human glutamate decarboxylases, 65-kDa GAD and 67-kDa GAD, are each encoded by a single gene

Interaction of nitric oxide synthase with the postsynaptic density protein PSD-95 and alpha1-syntrophin mediated by PDZ domains

PSD-95 is associated with the postsynaptic density and not with the presynaptic membrane at forebrain synapses

Domain interaction between NMDA receptor subunits and the postsynaptic density protein PSD-95

Distribution of NMDA and AMPA receptor subunits at thalamo-amygdaloid dendritic spines

Antidepressant effects of ketamine in depressed patients

A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression

Prefrontal cortical-amygdalar metabolism in major depression.

Expression, but not activity, of neuronal nitric oxide synthase is regionally increased in the alcoholic brain.

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143-153

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scholarly article

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10.1017/S1461145708008985

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2

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2645479

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