ArticleHuman molecular genetics2017
Homeostatic plasticity can be induced and expressed to restore synaptic strength at neuromuscular junctions undergoing ALS-related degeneration.
Article in Human molecular genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Elucidating the Role of Cerebellar Synaptic Dysfunction in C9orf72-ALS/FTD - a Systematic Review and Meta-Analysis.Cerebellum (London, England) · 2022Pooled it
- Glutamate receptor composition atbioRxiv : the preprint server for biology · 2026Article
- Selective regulation of transsynaptic alignment and postsynaptic assembly by a novel NCAM family synaptic adhesion molecule.bioRxiv : the preprint server for biology · 2026Article
- Article
- Nonionic signaling rapidly remodels postsynaptic DLG to induce retrograde homeostatic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Presynaptic Changes in Mouse Rod Photoreceptors During Early Retinitis Pigmentosa.Investigative ophthalmology & visual science · 2025Article
- Genetic dissection of theMolecular biology of the cell · 2025Article
- Distinct input-specific mechanisms enable presynaptic homeostatic plasticity.Science advances · 2025Article
- Tissue-specific knockout in the Drosophila neuromuscular system reveals ESCRT's role in formation of synapse-derived extracellular vesicles.PLoS genetics · 2024Article
- Distinct input-specific mechanisms enable presynaptic homeostatic plasticity.bioRxiv : the preprint server for biology · 2024Article
- Tissue-specific knockout inbioRxiv : the preprint server for biology · 2023Article
- Medium-Chain Fatty Acids Rescue Motor Function and Neuromuscular Junction Degeneration in aCells · 2023Article
- Article
- Physiologic and Nanoscale Distinctions Define Glutamatergic Synapses in Tonic vs Phasic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Article
- Neurexin and neuroligins jointly regulate synaptic degeneration at theFrontiers in cellular neuroscience · 2023Article
- A glutamate receptor C-tail recruits CaMKII to suppress retrograde homeostatic signaling.Nature communications · 2022Article
- Article
- The E3 ligase Thin controls homeostatic plasticity through neurotransmitter release repression.eLife · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is debilitating neurodegenerative disease characterized by motor neuron dysfunction and progressive weakening of the neuromuscular junction (NMJ). Hereditary ALS is strongly associated with variants in the human C9orf72 gene. We have characterized C9orf72 pathology at the Drosophila NMJ and utilized several approaches to restore synaptic strength in this model. First, we demonstrate a dramatic reduction in synaptic arborization and active zone number at NMJs following C9orf72 transgenic expression in motor neurons. Further, neurotransmission is similarly reduced at these synapses, consistent with severe degradation. However, despite these defects, C9orf72 synapses still retain the ability to express presynaptic homeostatic plasticity, a fundamental and adaptive form of NMJ plasticity in which perturbation to postsynaptic neurotransmitter receptors leads to a retrograde enhancement in presynaptic release. Next, we show that these endogenous but dormant homeostatic mechanisms can be harnessed to restore synaptic strength despite C9orf72 pathogenesis. Finally, activation of regenerative signaling is not neuroprotective in motor neurons undergoing C9orf72 toxicity. Together, these experiments define synaptic dysfunction at NMJs experiencing ALS-related degradation and demonstrate the potential to activate latent plasticity as a novel therapeutic strategy to restore synaptic strength.
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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.