Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice. - Wikidata - awgldk - TriplyDB

Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice.

Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G(93A-Low) mice.

http://www.wikidata.org/entity/Q43261428

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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 development Electrophysiologic biomarkers for assessing disease progression and the effect of riluzole in SOD1 G93A ALS mice Monoaminergic 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 ALS Comparison 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 signaling Effect 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 mice Evidence 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 model Intrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations.Lack of sigma-1 receptor exacerbates ALS progression in mice Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability Marked 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 sclerosis Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part II, results and discussion 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.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.

http://www.wikidata.org/entity/Q43261428

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2009 nî lūn-bûn

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2009年學術文章

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Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G

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Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.

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Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G

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Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.

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Early excitability changes in lumbar motoneurons of transgenic SOD1G85R and SOD1G

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Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.

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Journal of Neurophysiology

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Early excitability changes in ...... 1G85R and SOD1G(93A-Low) mice.

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Arnaud Pambo-Pambo

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Jacques Durand

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Jean-Patrick Gueritaud

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P2860

Aggregation and Motor Neuron Toxicity of an ALS-Linked SOD1 Mutant Independent from Wild-Type SOD1

Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS

Overloading of stable and exclusion of unstable human superoxide dismutase-1 variants in mitochondria of murine amyotrophic lateral sclerosis models

Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

ALS: a disease of motor neurons and their nonneuronal neighbors

Unraveling the mechanisms involved in motor neuron degeneration in ALS

Changes in the spinal cord proteome of an amyotrophic lateral sclerosis murine model determined by differential in-gel electrophoresis.

Perinatal development of lumbar motoneurons and their inputs in the rat.

Familial amyotrophic lateral sclerosis.

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3627-3642

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10.1152/JN.00482.2009

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102

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2009-10-14T00:00:00Z

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19828728

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