Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis.
about
Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and DiseaseModeling ALS with motor neurons derived from human induced pluripotent stem cellsExperimental Design and Data Analysis Issues Contribute to Inconsistent Results of C-Bouton Changes in Amyotrophic Lateral Sclerosis.Motor neuron vulnerability and resistance in amyotrophic lateral sclerosis.Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons.Developing electrical properties of postnatal mouse lumbar motoneurons.Potassium currents dynamically set the recruitment and firing properties of F-type motoneurons in neonatal micePostactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice.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 sclerosisInhibitory dysfunction in amyotrophic lateral sclerosis: future therapeutic opportunities.Modeling the C9ORF72 repeat expansion mutation using human induced pluripotent stem cells.Impairments in Motor Neurons, Interneurons and Astrocytes Contribute to Hyperexcitability in ALS: Underlying Mechanisms and Paths to Therapy.New perspectives on amyotrophic lateral sclerosis: the role of glial cells at the neuromuscular junction.Axonal Excitability in Amyotrophic Lateral Sclerosis : Axonal Excitability in ALS.4-Aminopyridine Induced Activity Rescues Hypoexcitable Motor Neurons from Amyotrophic Lateral Sclerosis Patient-Derived Induced Pluripotent Stem Cells.Aberrant association of misfolded SOD1 with Na(+)/K(+)ATPase-α3 impairs its activity and contributes to motor neuron vulnerability in ALS.Is hyperexcitability really guilty in amyotrophic lateral sclerosis?A Stem Cell Model of the Motor Circuit Uncouples Motor Neuron Death from Hyperexcitability Induced by SMN Deficiency.Direct Lineage Reprogramming Reveals Disease-Specific Phenotypes of Motor Neurons from Human ALS Patients.Motor Areas Show Altered Dendritic Structure in an Amyotrophic Lateral Sclerosis Mouse Model.Escape from homeostasis: spinal microcircuits and progression of amyotrophic lateral sclerosis.Chronic electromyograms in treadmill running SOD1 mice reveal early changes in muscle activation.Changes in the Excitability of Neocortical Neurons in a Mouse Model of Amyotrophic Lateral Sclerosis Are Not Specific to Corticospinal Neurons and Are Modulated by Advancing Disease.Sigma-1 Receptor in Motoneuron Disease.The vulnerability of spinal motoneurons and soma size plasticity in a mouse model of amyotrophic lateral sclerosis.Kv1.2 Channels Promote Nonlinear Spiking Motoneurons for Powering Up Locomotion.Recurrent excitation between motoneurones propagates across segments and is purely glutamatergic.Amyotrophic Lateral Sclerosis (ALS) and Adenosine Receptors.Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS.Marking the differences in motoneurons.
P2860
Q26769059-A715945F-3756-4E93-BA6F-1C3A960DF929Q28076026-6A8C1C6E-B2E3-49ED-AD6C-B05D0B026C9EQ31155328-B430BE0D-EDA0-4B0E-8003-F805CCA3C76DQ33665800-173ED037-F5B7-49C6-BBFB-2D98933678A3Q35357235-FD505C12-5A76-4DBD-A08B-0C5E33DCBB0BQ36018256-BA32F2E2-5F0E-4F2D-AF57-482790194A8DQ36084199-E28B9A58-F62C-451D-8ADB-248AC406A88CQ36496962-0CF078A1-71A3-49D6-A901-EE2E0A72F7A9Q37150806-E06FFC5A-1E0C-4122-B216-CC6D861AF92EQ38653220-3AB48A4B-5D6F-40E9-9114-77D6559476DDQ38741408-75A15CE9-2718-404F-94A7-25CFE9A2511DQ38761708-9EFEE95C-FAE9-40B8-9F79-2C039D1BC875Q38955746-88C842CE-C4B3-49EE-B3A1-9032FC59C06AQ39017694-E3C7B5A0-7818-4BE5-8ACE-D5AA5756F284Q39945217-24471A71-BE80-49CA-95E7-C948846B8B9CQ41087321-05E7CA28-81FC-4F30-94A7-4B9B9CFF8D4FQ41817857-95F02DC9-85BA-4EF2-8E5E-A6C63A0B1A90Q41885598-82FF710C-CF7C-4321-AA9F-21B74DC5F4EDQ43098018-4FEA55EF-43AC-454B-81A2-4BED08651D04Q47118168-9AAF7CA3-BBFE-4D32-8E9A-443C2F37C816Q47642795-7E0DE114-4822-407C-9622-7DD63B9E01CBQ48099230-4D6B272B-C77D-4654-8636-516BFA71DFE1Q48148996-16EA1EF8-8387-4AF9-91C1-3D3E73D4FEABQ48258033-8E678708-0D4D-4501-8AE6-EAD4F4684960Q52675413-2B9385B0-5A14-44E0-AC3B-985B07696818Q54970000-FA0F64CE-7258-4D15-93A7-7B64A094F002Q54976166-5E6D6ED2-29D6-4AFD-AB10-A43B1E8A10A7Q55003224-A72C3C00-0A5F-474C-B92B-72EFADA85C1BQ55215170-C142764E-16B0-4941-A34A-77AB076701A8Q55296515-85EDD959-7E8A-413D-8C87-BA75F17AF490
P2860
Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
Early intrinsic hyperexcitabil ...... amyotrophic lateral sclerosis.
@en
type
label
Early intrinsic hyperexcitabil ...... amyotrophic lateral sclerosis.
@en
prefLabel
Early intrinsic hyperexcitabil ...... amyotrophic lateral sclerosis.
@en
P2860
P50
P356
P1433
P1476
Early intrinsic hyperexcitabil ...... amyotrophic lateral sclerosis
@en
P2093
Rebecca D Imhoff-Manuel
P2860
P356
10.7554/ELIFE.04046
P407
P577
2014-10-14T00:00:00Z