ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Signaling events in axons and/or dendrites render motor neurons vulnerable to mutant superoxide dismutase toxicity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Identification of Therapeutic Targets for Amyotrophic Lateral Sclerosis Using PandaOmics - An AI-Enabled Biological Target Discovery Platform.Frontiers in aging neuroscience · 2022Article
- The Role of Altered BDNF/TrkB Signaling in Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2019Review
- Impaired Mitophagy Plays a Role in Denervation of Neuromuscular Junctions in ALS Mice.Frontiers in neuroscience · 2017Article
- Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and Disease.Neural plasticity · 2016Review
- Inhibition of Cytohesins Protects against Genetic Models of Motor Neuron Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease.Human molecular genetics · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The survival of dorsal root ganglion and sympathetic neurons is promoted whether nerve growth factor (NGF) activates TrkA receptors on the cell body or the axon. Yet other aspects of neurotrophic factor actions (i.e., ability to promote axon growth, selection of neurochemical phenotype and engagement of signaling modules) differ as a function of the location of the ligand-receptor interaction. The extent to which these observations are relevant to CNS neurons is unknown. This may be particularly relevant to neurodegenerative diseases such as amyotrophic lateral sclerosis, where beneficial axon-target interactions are disturbed early in the disease process. Here we characterize the growth of pure motor neurons in compartment cultures and show that brain-derived neurotrophic factor (BDNF) stimulation of the cell body or axons/dendrites promotes survival. Expression of G37R mutant superoxide dismutase (SOD) in motor neurons will lead to death and this depends on BDNF activation of TrkB on axons and/or dendrites. BDNF action depends upon endocytosis of the BDNF-TrkB complex and de novo protein synthesis. These results highlight the importance of signaling events occurring in axons/dendrites in mutant SOD toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.