Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice.
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Stronger is not always better: could a bodybuilding dietary supplement lead to ALS?Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.Characterization of a novel SOD-1(G93A) transgenic mouse line with very decelerated disease developmentElectrophysiologic biomarkers for assessing disease progression and the effect of riluzole in SOD1 G93A ALS miceMonoaminergic control of spinal locomotor networks in SOD1G93A newborn mice.Effect of fluoxetine on disease progression in a mouse model of ALS.Persistent inward currents in spinal motoneurons: important for normal function but potentially harmful after spinal cord injury and in amyotrophic lateral sclerosis.Selective degeneration of a physiological subtype of spinal motor neuron in mice with SOD1-linked ALSComparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Clinical Measures of Disease Progression in 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.Developing electrical properties of postnatal mouse lumbar motoneurons.Potassium currents dynamically set the recruitment and firing properties of F-type motoneurons in neonatal miceEvidence from computer simulations for alterations in the membrane biophysical properties and dendritic processing of synaptic inputs in mutant superoxide dismutase-1 motoneurons.ALS biomarkers for therapy development: State of the field and future directions.State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model.Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish modelIntrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations.Lack of sigma-1 receptor exacerbates ALS progression in miceMutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitabilityMarked 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 sclerosisCharacterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part II, results and discussionGamma 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.SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments.Motor unit.Inhibitory dysfunction in amyotrophic lateral sclerosis: future therapeutic opportunities.Sigma-1 (σ1) Receptor in Memory and Neurodegenerative Diseases.Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.Aberrant association of misfolded SOD1 with Na(+)/K(+)ATPase-α3 impairs its activity and contributes to motor neuron vulnerability in ALS.Voltage-gated calcium channels are abnormal in cultured spinal motoneurons in the G93A-SOD1 transgenic mouse model of ALS.Early pathogenesis in the adult-onset neurodegenerative disease amyotrophic lateral sclerosis.Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis.Shortcomings in the Current Amyotrophic Lateral Sclerosis Trials and Potential Solutions for Improvement.Pre- and postsynaptic mechanisms underlying inhibition of hypoglossal motor neuron excitability by riluzole.SOD1 Mutations Causing Familial Amyotrophic Lateral Sclerosis Induce Toxicity in Astrocytes: Evidence for Bystander Effects in a Continuum of Astrogliosis.Motor Areas Show Altered Dendritic Structure in an Amyotrophic Lateral Sclerosis Mouse Model.Chronic electromyograms in treadmill running SOD1 mice reveal early changes in muscle activation.Sigma-1 Receptor in Motoneuron Disease.
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Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh-hant
name
Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G
@nl
Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.
@en
type
label
Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G
@nl
Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.
@en
prefLabel
Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G
@nl
Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.
@en
P2093
P2860
P356
P1476
Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.
@en
P2093
Arnaud Pambo-Pambo
Jacques Durand
Jean-Patrick Gueritaud
P2860
P304
P356
10.1152/JN.00482.2009
P407
P577
2009-10-14T00:00:00Z