Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression.
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The Emergence of NMDA Receptor Metabotropic Function: Insights from ImagingNon-ionotropic signaling by the NMDA receptor: controversy and opportunityAmyloid-β-Induced Dysregulation of AMPA Receptor TraffickingWnts in action: from synapse formation to synaptic maintenanceA Metabotropic-Like Flux-Independent NMDA Receptor Regulates Ca2+ Exit from Endoplasmic Reticulum and Mitochondrial Membrane Potential in Cultured AstrocytesAlzheimer's therapeutics targeting amyloid beta 1-42 oligomers I: Abeta 42 oligomer binding to specific neuronal receptors is displaced by drug candidates that improve cognitive deficitsSurface dynamics of GluN2B-NMDA receptors controls plasticity of maturing glutamate synapsesAlzheimer's therapeutics targeting amyloid beta 1-42 oligomers II: Sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicityFocusing the amyloid cascade hypothesis on N-truncated Abeta peptides as drug targets against Alzheimer's diseaseAmyloid β Protein and Alzheimer's Disease: When Computer Simulations Complement Experimental Studies.Age-Dependent Modifications of AMPA Receptor Subunit Expression Levels and Related Cognitive Effects in 3xTg-AD Mice.Regulation of neuronal gene expression and survival by basal NMDA receptor activity: a role for histone deacetylase 4.Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivoTau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β.Non-Ionotropic NMDA Receptor Signaling Drives Activity-Induced Dendritic Spine Shrinkage.Conformational signaling required for synaptic plasticity by the NMDA receptor complexCalcium flux-independent NMDA receptor activity is required for Aβ oligomer-induced synaptic lossIncreasing the Receptor Tyrosine Kinase EphB2 Prevents Amyloid-β-induced Depletion of Cell Surface Glutamate Receptors by a Mechanism That Requires the PDZ-binding Motif of EphB2 and Neuronal Activity.Metabotropic NMDA receptor function is required for NMDA receptor-dependent long-term depression.Inhibiting BACE1 to reverse synaptic dysfunctions in Alzheimer's disease.Glycine triggers a non-ionotropic activity of GluN2A-containing NMDA receptors to confer neuroprotection.Glycine Potentiates AMPA Receptor Function through Metabotropic Activation of GluN2A-Containing NMDA Receptors.Amyloid-β effects on synapses and memory require AMPA receptor subunit GluA3.Local and Use-Dependent Effects of β-Amyloid Oligomers on NMDA Receptor Function Revealed by Optical Quantal Analysis.NMDA receptor as a newly identified member of the metabotropic glutamate receptor family: clinical implications for neurodegenerative diseases.Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer's diseaseEmerging Synaptic Molecules as Candidates in the Etiology of Neurological Disorders.Ionotropic NMDA receptor signaling is required for the induction of long-term depression in the mouse hippocampal CA1 region.A 'danse macabre': tau and Fyn in STEP with amyloid beta to facilitate induction of synaptic depression and excitotoxicity.Possible contributions of a novel form of synaptic plasticity in Aplysia to reward, memory, and their dysfunctions in mammalian brain.The developmental stages of synaptic plasticity.AMPA-silent synapses in brain development and pathology.CaMKII: claiming center stage in postsynaptic function and organization.Reciprocal disruption of neuronal signaling and Aβ production mediated by extrasynaptic NMDA receptors: a downward spiral.Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.The Role of Reelin Signaling in Alzheimer's Disease.Synapto-depressive effects of amyloid beta require PICK1Posttranslational modification impact on the mechanism by which amyloid-β induces synaptic dysfunction.
P2860
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P2860
Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@ast
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@en
type
label
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@ast
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@en
prefLabel
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@ast
Metabotropic NMDA receptor fun ...... d-induced synaptic depression.
@en
P2860
P356
P1476
Metabotropic NMDA receptor function is required for β-amyloid-induced synaptic depression
@en
P2093
Roberto Malinow
P2860
P304
P356
10.1073/PNAS.1219605110
P407
P577
2013-02-19T00:00:00Z