Cell death after spinal cord injury is exacerbated by rapid TNF alpha-induced trafficking of GluR2-lacking AMPARs to the plasma membrane
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Menopause, obesity and inflammation: interactive risk factors for Alzheimer's diseaseTumor necrosis factor alpha: a link between neuroinflammation and excitotoxicityA Neurologist's Guide to TNF Biology and to the Principles behind the Therapeutic Removal of Excess TNF in DiseaseNeurotrauma and inflammation: CNS and PNS responsesTopiramate treatment is neuroprotective and reduces oligodendrocyte loss after cervical spinal cord injuryDerivation of multivariate syndromic outcome metrics for consistent testing across multiple models of cervical spinal cord injury in ratsAnalyzing dendritic spine pathology in Alzheimer's disease: problems and opportunitiesA perspective on the role of class III semaphorin signaling in central nervous system traumaAmyloid β: one of three danger-associated molecules that are secondary inducers of the proinflammatory cytokines that mediate Alzheimer's diseaseGlial tumor necrosis factor alpha (TNFα) generates metaplastic inhibition of spinal learningPharmacological Investigation of Fluoro-Gold Entry into Spinal NeuronsSecreted phospholipase A2 involvement in neurodegeneration: differential testing of prosurvival and anti-inflammatory effects of enzyme inhibitionSyndromics: a bioinformatics approach for neurotrauma researchGrowth factors in synaptic function.Cannabinoid receptor activation reduces TNFalpha-induced surface localization of AMPAR-type glutamate receptors and excitotoxicity.Topological data analysis for discovery in preclinical spinal cord injury and traumatic brain injury.Beneficial effects of secretory leukocyte protease inhibitor after spinal cord injury.Hippocampal TNFα Signaling Contributes to Seizure Generation in an Infection-Induced Mouse Model of Limbic Epilepsy.ProNGF induces TNFalpha-dependent death of retinal ganglion cells through a p75NTR non-cell-autonomous signaling pathwayPeripheral inflammation induces tumor necrosis factor dependent AMPA receptor trafficking and Akt phosphorylation in spinal cord in addition to pain behaviorThe Irvine, Beatties, and Bresnahan (IBB) Forelimb Recovery Scale: An Assessment of Reliability and Validity.The meteorology of cytokine storms, and the clinical usefulness of this knowledgeDifferential distribution of PI3K isoforms in spinal cord and dorsal root ganglia: potential roles in acute inflammatory painCentral but not systemic administration of XPro1595 is therapeutic following moderate spinal cord injury in miceTNF-α contributes to spinal cord synaptic plasticity and inflammatory pain: distinct role of TNF receptor subtypes 1 and 2.Peripheral noxious stimulation reduces withdrawal threshold to mechanical stimuli after spinal cord injury: role of tumor necrosis factor alpha and apoptosis.Targeted overexpression of mitochondrial catalase prevents radiation-induced cognitive dysfunction.Inflammation alters trafficking of extrasynaptic AMPA receptors in tonically firing lamina II neurons of the rat spinal dorsal horn.Tight squeeze, slow burn: inflammation and the aetiology of cervical myelopathy.Leveraging biomedical informatics for assessing plasticity and repair in primate spinal cord injury.Genetic deletion of TNF receptor suppresses excitatory synaptic transmission via reducing AMPA receptor synaptic localization in cortical neurons.Modulation of spinal cord synaptic activity by tumor necrosis factor α in a model of peripheral neuropathyEthanol dose-dependently elicits opposing regulatory effects on hippocampal AMPA receptor GluA2 subunits through a zeta inhibitory peptide-sensitive kinase in adolescent and adult Sprague-Dawley rats.Tumor necrosis factor alpha mediates GABA(A) receptor trafficking to the plasma membrane of spinal cord neurons in vivo.Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice.Central nociceptive sensitization vs. spinal cord training: opposing forms of plasticity that dictate function after complete spinal cord injuryThe role of mTOR signaling pathway in spinal cord injury.Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury.AMPA Receptor Phosphorylation and Synaptic Colocalization on Motor Neurons Drive Maladaptive Plasticity below Complete Spinal Cord Injury.TNF-α triggers rapid membrane insertion of Ca(2+) permeable AMPA receptors into adult motor neurons and enhances their susceptibility to slow excitotoxic injury.
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P2860
Cell death after spinal cord injury is exacerbated by rapid TNF alpha-induced trafficking of GluR2-lacking AMPARs to the plasma membrane
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
@pt
bilimsel makale
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scientific article published on October 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Cell death after spinal cord i ...... AMPARs to the plasma membrane
@en
Cell death after spinal cord i ...... AMPARs to the plasma membrane.
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type
label
Cell death after spinal cord i ...... AMPARs to the plasma membrane
@en
Cell death after spinal cord i ...... AMPARs to the plasma membrane.
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prefLabel
Cell death after spinal cord i ...... AMPARs to the plasma membrane
@en
Cell death after spinal cord i ...... AMPARs to the plasma membrane.
@nl
P2093
P2860
P50
P1476
Cell death after spinal cord i ...... AMPARs to the plasma membrane
@en
P2093
Brandon A Miller
Eric C Beattie
Jacqueline C Bresnahan
Michael S Beattie
P2860
P304
11391-11400
P356
10.1523/JNEUROSCI.3708-08.2008
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P577
2008-10-01T00:00:00Z