ArticleeLife2016
A novel synaptic plasticity rule explains homeostasis of neuromuscular transmission.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed.
- Transsynaptic linking of calcium channels and postsynaptic receptors at a dyadic synapse.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Microelectrode-based approaches for studying cholinergic neuromuscular transmission.Biophysical reviews · 2025Review
- Review
- Postsynaptic receptors regulate presynaptic transmitter stability through transsynaptic bridges.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Application of digital tools and artificial intelligence in the Myasthenia Gravis Core Examination.Frontiers in neurology · 2024Article
- Neuromuscular junction transmission failure in aging and sarcopenia: The nexus of the neurological and muscular systems.Ageing research reviews · 2023Review
- ACh Transfers: Homeostatic Plasticity of Cholinergic Synapses.Cellular and molecular neurobiology · 2023Review
- Neuromuscular recovery from botulism involves multiple forms of compensatory plasticity.Frontiers in cellular neuroscience · 2023Article
- Autonomic Nerve Fibers Aberrantly Reinnervate Denervated Facial Muscles and Alter Muscle Fiber Population.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Role of α7 Nicotinic Acetylcholine Receptors in Synaptic Transmission in Frog Neuromuscular Contacts.Bulletin of experimental biology and medicine · 2022Article
- Distinct molecular pathways govern presynaptic homeostatic plasticity.Cell reports · 2021Article
- Evidence That the Central Nervous System Can Induce a Modification at the Neuromuscular Junction That Contributes to the Maintenance of a Behavioral Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The TOR Pathway at the Neuromuscular Junction: More Than a Metabolic Player?Frontiers in molecular neuroscience · 2020Review
- Synthetic Pinnatoxins A and G Reversibly Block Mouse Skeletal Neuromuscular Transmission In Vivo and In Vitro.Marine drugs · 2019Article
- Muscle Nicotinic Acetylcholine Receptors May Mediate Trans-Synaptic Signaling at the Mouse Neuromuscular Junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Functional consequences of pre- and postsynaptic expression of synaptic plasticity.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- A Gradient in Synaptic Strength and Plasticity among Motoneurons Provides a Peripheral Mechanism for Locomotor Control.Current biology : CB · 2017Article
- A Novel Egr-1-Agrin Pathway and Potential Implications for Regulation of Synaptic Physiology and Homeostasis at the Neuromuscular Junction.Frontiers in aging neuroscience · 2017Article
- Morphological Regeneration and Functional Recovery of Neuromuscular Junctions after Tourniquet-Induced Injuries in Mouse Hindlimb.Frontiers in physiology · 2017Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excitability differs among muscle fibers and undergoes continuous changes during development and growth, yet the neuromuscular synapse maintains a remarkable fidelity of execution. Here we show in two evolutionarily distant vertebrates (Xenopus laevis cell culture and mouse nerve-muscle ex-vivo) that the skeletal muscle cell constantly senses, through two identified calcium signals, synaptic events and their efficacy in eliciting spikes. These sensors trigger retrograde signal(s) that control presynaptic neurotransmitter release, resulting in synaptic potentiation or depression. In the absence of spikes, synaptic events trigger potentiation. Once the synapse is sufficiently strong to initiate spiking, the occurrence of these spikes activates a negative retrograde feedback. These opposing signals dynamically balance the synapse in order to continuously adjust neurotransmitter release to a level matching current muscle cell excitability.
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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.