Neonatal neuronal circuitry shows hyperexcitable disturbance in a mouse model of the adult-onset neurodegenerative disease amyotrophic lateral sclerosis
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Stronger is not always better: could a bodybuilding dietary supplement lead to ALS?Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and DiseaseINaP selective inhibition reverts precocious inter- and motorneurons hyperexcitability in the Sod1-G93R zebrafish ALS modelInhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.Modeling ALS with motor neurons derived from human induced pluripotent stem cellsALS as a distal axonopathy: molecular mechanisms affecting neuromuscular junction stability in the presymptomatic stages of the diseaseMolecular chaperone Hsp110 rescues a vesicle transport defect produced by an ALS-associated mutant SOD1 protein in squid axoplasm.Effect of fluoxetine on disease progression in a mouse model of ALS.Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).A review of the neural mechanisms of action and clinical efficiency of riluzole in treating amyotrophic lateral sclerosis: what have we learned in the last decade?Persistent inward currents in spinal motoneurons: important for normal function but potentially harmful after spinal cord injury and in amyotrophic lateral sclerosis.Progressive changes in synaptic inputs to motoneurons in adult sacral spinal cord of a mouse model of amyotrophic lateral sclerosisAdenosine monophosphate-activated protein kinase activation enhances embryonic neural stem cell apoptosis in a mouse model of amyotrophic lateral sclerosis.An ALS-Associated Mutant SOD1 Rapidly Suppresses KCNT1 (Slack) Na+-Activated K+ Channels in Aplysia NeuronsSoma size and Cav1.3 channel expression in vulnerable and resistant motoneuron populations of the SOD1G93A mouse model of ALS.Glycine receptor channels in spinal motoneurons are abnormal in a transgenic mouse model of amyotrophic lateral sclerosis.Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viabilityIdentifying the primary site of pathogenesis in amyotrophic lateral sclerosis - vulnerability of lower motor neurons to proximal excitotoxicity.Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Motoneuron subtypes show specificity in glycine receptor channel abnormalities in a transgenic mouse model of amyotrophic lateral sclerosis.Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signalingEffect of prolonged riluzole exposure on cultured motoneurons in a mouse model of ALS.Evidence from computer simulations for alterations in the membrane biophysical properties and dendritic processing of synaptic inputs in mutant superoxide dismutase-1 motoneurons.Postactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice.Inducing Chronic Excitotoxicity in the Mouse Spinal Cord to Investigate Lower Motor Neuron Degeneration.Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitabilityMutant SOD1 protein increases Nav1.3 channel excitabilityMarked changes in dendritic structure and spine density precede significant neuronal death in vulnerable cortical pyramidal neuron populations in the SOD1(G93A) mouse model of amyotrophic lateral sclerosisA method for the three-dimensional reconstruction of Neurobiotin™-filled neurons and the location of their synaptic inputs.Developmental changes in the morphology of mouse hypoglossal motor neuronsDefects in synapse structure and function precede motor neuron degeneration in Drosophila models of FUS-related ALS.Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part II, results and discussionFast kinetics, high-frequency oscillations, and subprimary firing range in adult mouse spinal motoneurons.Cortical synaptic and dendritic spine abnormalities in a presymptomatic TDP-43 model of amyotrophic lateral sclerosis.Increased Synaptic Excitation and Abnormal Dendritic Structure of Prefrontal Cortex Layer V Pyramidal Neurons following Prolonged Binge-Like Consumption of Ethanol.Gamma motor neurons survive and exacerbate alpha motor neuron degeneration in ALS.Astrocytes expressing mutant SOD1 and TDP43 trigger motoneuron death that is mediated via sodium channels and nitroxidative stress.Calretinin and Neuropeptide Y interneurons are differentially altered in the motor cortex of the SOD1G93A mouse model of ALS.SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments.Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis.
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Neonatal neuronal circuitry shows hyperexcitable disturbance in a mouse model of the adult-onset neurodegenerative disease amyotrophic lateral sclerosis
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on October 2008
@en
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
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis
@en
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis.
@nl
type
label
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis
@en
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis.
@nl
prefLabel
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis
@en
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis.
@nl
P2093
P2860
P50
P1476
Neonatal neuronal circuitry sh ...... amyotrophic lateral sclerosis
@en
P2093
Brigitte van Zundert
Marieke H Peuscher
Mark C Bellingham
Meri Hynynen
Rachael L Neve
P2860
P304
10864-10874
P356
10.1523/JNEUROSCI.1340-08.2008
P407
P577
2008-10-01T00:00:00Z