ArticleThe Journal of physiology2005
Reactive oxygen species contribute to the presynaptic action of extracellular ATP at the frog neuromuscular junction.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 61 citations in OpenAlex.
- 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
- Mechanism of Purinergic Regulation of Neurotransmission in Mouse Neuromuscular Junction: The Role of Redox Signaling and Lipid Rafts.Neurochemical research · 2024Article
- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- Human Neuromuscular Junction on a Chip: Impact of Amniotic Fluid Stem Cell Extracellular Vesicles on Muscle Atrophy and NMJ Integrity.International journal of molecular sciences · 2023Article
- L-type CaCellular and molecular neurobiology · 2022Article
- Learning from magnetotactic bacteria:Frontiers in cellular neuroscience · 2022Article
- Purinergic signaling in the modulation of redox biology.Redox biology · 2021Review
- Modulatory Roles of ATP and Adenosine in Cholinergic Neuromuscular Transmission.International journal of molecular sciences · 2020Review
- Aberrant redox signalling and stress response in age-related muscle decline: Role in inter- and intra-cellular signalling.Free radical biology & medicine · 2019Review
- Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans.Cell stress & chaperones · 2016Article
- The antioxidant requirement for plasma membrane repair in skeletal muscle.Free radical biology & medicine · 2015Article
- Homocysteine aggravates ROS-induced depression of transmitter release from motor nerve terminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia.Frontiers in cellular neuroscience · 2015Article
- Role of membrane cholesterol in spontaneous exocytosis at frog neuromuscular synapses: reactive oxygen species-calcium interplay.The Journal of physiology · 2014Article
- An intracellular redox sensor for reactive oxygen species at the M3-M4 linker of GABAA ρ1 receptors.British journal of pharmacology · 2014Article
- The role of oxidative stress in degeneration of the neuromuscular junction in amyotrophic lateral sclerosis.Frontiers in cellular neuroscience · 2014Review
- Purinergic signalling in the musculoskeletal system.Purinergic signalling · 2013Review
- The novel TrkB receptor agonist 7,8-dihydroxyflavone enhances neuromuscular transmission.Muscle & nerve · 2012Article
- Gender-Specific Mechanism of Synaptic Impairment and Its Prevention by GCSF in a Mouse Model of ALS.Frontiers in cellular neuroscience · 2011Article
- The role of cholesterol in the exo- and endocytosis of synaptic vesicles in frog motor nerve endings.Neuroscience and behavioral physiology · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During normal cell metabolism the production of intracellular ATP is associated with the generation of reactive oxygen species (ROS), which appear to be important signalling molecules. Both ATP and ROS can be released extracellularly by skeletal muscle during intense activity. Using voltage clamp recording combined with imaging and biochemical assay of ROS, we tested the hypothesis that at the neuromuscular junction extracellular ATP generates ROS to inhibit transmitter release from motor nerve endings. We found that ATP produced the presynaptic inhibitory action on multiquantal end-plate currents. The inhibitory action of ATP (but not that of adenosine) was significantly reduced by several antioxidants or extracellular catalase, which breaks down H2O2. Consistent with these data, the depressant effect of ATP was dramatically potentiated by the pro-oxidant Fe2+. Exogenous H2O2 reproduced the depressant effects of ATP and showed similar sensitivity to anti- and pro-oxidants. While NO also inhibited synaptic transmission, inhibitors of the NO-producing cascade did not prevent the depressant action of ATP. The ferrous oxidation in xylenol orange assay showed the increase of ROS production by ATP and 2-MeSADP but not by adenosine. Suramin, a non-selective antagonist of P2 receptors, and pertussis toxin prevented the action of ATP on ROS production. Likewise, imaging with the ROS-sensitive dye carboxy-2',7'-dichlorodihydrofluorescein revealed increased production of ROS in the muscle treated with ATP or ADP while UTP or adenosine had no effect. Thus, generation of ROS contributed to the ATP-mediated negative feedback mechanism controlling quantal secretion of ACh from the motor nerve endings.
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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.