ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Skeletal muscle calpain acts through nitric oxide and neural miRNAs to regulate acetylcholine release in motor nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Influence of nitrate supplementation on motor unit activity during recovery following a sustained ischemic contraction in recreationally active young males.European journal of nutrition · 2024Trial
- Effect of nitrate supplementation on skeletal muscle motor unit activity during isometric blood flow restriction exercise.European journal of applied physiology · 2022Trial
- Frequency-Dependent Mechanism of 24-Hydroxycholesterol-Mediated Modulation of Neurotransmitter Release at the Mouse Neuromuscular Junction: The Role of Reactive Oxygen Species.Neurochemical research · 2025Article
- Signature of miRNAs derived from the circulating exosomes of patients with amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2023Article
- MicroRNA-137-3p Protects PC12 Cells Against Oxidative Stress by Downregulation of Calpain-2 and nNOS.Cellular and molecular neurobiology · 2021Article
- Article
- MicroRNA-183-5p is stress-inducible and protects neurons against cell death in amyotrophic lateral sclerosis.Journal of cellular and molecular medicine · 2020Article
- Glutamate at the Vertebrate Neuromuscular Junction: From Modulation to Neurotransmission.Cells · 2019Review
- Differential Expression of Several miRNAs and the Host GenesFrontiers in molecular neuroscience · 2018Article
- Exosomes from NSC-34 Cells Transfected with hSOD1-G93A Are Enriched in miR-124 and Drive Alterations in Microglia Phenotype.Frontiers in neuroscience · 2017Article
- Downregulation ofFrontiers in molecular neuroscience · 2017Article
- Neuromuscular Junctions as Key Contributors and Therapeutic Targets in Spinal Muscular Atrophy.Frontiers in neuroanatomy · 2016Review
- Identification of plasma microRNAs as a biomarker of sporadic Amyotrophic Lateral Sclerosis.Molecular brain · 2015Article
- Fluoxetine is neuroprotective in slow-channel congenital myasthenic syndrome.Experimental neurology · 2015Article
- SMN regulates axonal local translation via miR-183/mTOR pathway.Human molecular genetics · 2014Article
- The role of miRNA in motor neuron disease.Frontiers in cellular neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cholinergic overactivity in diseases of neuromuscular transmission elicits a retrograde signal resembling homeostatic synaptic plasticity that downregulates transmitter release. Understanding this compensatory pathway could provide insights into novel therapeutic avenues and molecular mechanisms underlying learning and memory. Here we identify nitric oxide as a possible source of this signal in pathological human and mouse muscle samples and link this signaling pathway to changes in synaptic function in the neuromuscular junction. We further show that neuronal nitric oxide synthase is regulated by cholinergic excess through activation of skeletal muscle calpain and its effect on Cdk5 and CaMKII, leading to direct modulation of presynaptic function. Finally, we show that this signaling pathway acts through specific miRNA control of presynaptic vesicle protein expression. The control of presynaptic miRNA levels by postsynaptic activity represents a novel mechanism for the modulation of synaptic activity in normal or pathological conditions.
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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.