ArticleThe Journal of physiology2003
Dual action of hydrogen peroxide on synaptic transmission at the frog neuromuscular junction.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- N-acetylcysteine manipulation fails to elicit an increase in glutathione in a teleost model.Fish physiology and biochemistry · 2018Trial
- Expression, localization and regulation of NADPH oxidases in pancreatic beta cells.Redox report : communications in free radical research · 2025Article
- 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
- Article
- Endogenous hydrogen peroxide positively regulates secretion of a gut-derived peptide in neuroendocrine potentiation of the oxidative stress response inbioRxiv : the preprint server for biology · 2024Article
- 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
- Hydrogen peroxide suppresses excitability of gonadotropin-releasing hormone neurons in adult mouse.Frontiers in endocrinology · 2022Article
- Mitochondrial hydrogen peroxide positively regulates neuropeptide secretion during diet-induced activation of the oxidative stress response.Nature communications · 2021Article
- Mitochondrial oxidative stress impairs contractile function but paradoxically increases muscle mass via fibre branching.Journal of cachexia, sarcopenia and muscle · 2019Article
- Homocysteine sensitizes the mouse neuromuscular junction to oxidative stress by nitric oxide.Neuroreport · 2018Article
- Advances in cellular and integrative control of oxygen homeostasis within the central nervous system.The Journal of physiology · 2018Review
- Regulation of neuronal development and function by ROS.FEBS letters · 2018Review
- 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
- Evidence of a common mechanism of disassembly of adherens junctions through Gα13 targeting of VE-cadherin.The Journal of experimental medicine · 2014Article
- The role of oxidative stress in degeneration of the neuromuscular junction in amyotrophic lateral sclerosis.Frontiers in cellular neuroscience · 2014Review
- Effect of hydrogen peroxide on electrical coupling between identified Lymnaea neurons.Invertebrate neuroscience : IN · 2012Article
- SNAP-25 contains non-acylated thiol pairs that can form intrachain disulfide bonds: possible sites for redox modulation of neurotransmission.Cellular and molecular neurobiology · 2012Article
- Hydrogen peroxide differentially affects activity in the pre-Bötzinger complex and hippocampus.Journal of neurophysiology · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is evidence that reactive oxygen species (ROS) are produced and released during neuromuscular activity, but their role in synaptic transmission is not known. Using a two-electrode voltage-clamp technique, at frog neuromuscular junctions, the action H2O2 on end-plate currents (EPC) was studied to determine the targets for this membrane-permeable ROS. In curarized or cut muscles, micromolar concentrations of H2O2 increased the amplitude of EPCs. Higher (> 30 microM) doses inhibited EPCs and prolonged current decay. These effects were presynaptic since H2O2 did not change the amplitude or duration of miniature EPCs (although it reduced the rate of spontaneous release at high concentrations). Quantal analysis and deconvolution methods showed that facilitation of EPCs was due to increased quantal release, while depression was accompanied by temporal dispersion of evoked release. Extracellular recordings revealed prolonged presynaptic Ca2+ entry in the presence of high H2O2. Both low and high H2O2 increased presynaptic potentiation during high-frequency stimulation. Pro-oxidant Fe2+ did not affect facilitation by low doses of H2O2 but augmented the inhibition of EPCs by high H2O2, indicating involvement of hydroxyl radicals. High Mg2+ and the ROS scavenger N-acetylcysteine eliminated both the facilitatory and depressant effects of H2O2. The facilitatory effect of H2O2 was prevented by protein kinase C (PKC) inhibitors and 4beta-phorbol 12-myristate, 13-acetate (PMA), an activator of PKC. PKC inhibitors but not PMA also abolished the depressant effect of H2O2. Our data suggest complex presynaptic actions of H2O2, which could serve as a fast feedback modulator of intense neuromuscular transmission.
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