Action of Hydrogen Peroxide on Synaptic Transmission at the Mouse Neuromuscular Junction
Autor: | Alexey M. Petrov, A. R. Giniatullin, Rashid Giniatullin |
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Rok vydání: | 2019 |
Předmět: |
Male
0301 basic medicine Diaphragm Neuromuscular Junction Neurotransmission Synaptic Transmission Antioxidants Exocytosis Neuromuscular junction Tissue Culture Techniques Tosyl Compounds Membrane Lipids Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Lipid oxidation medicine Animals Neurotransmitter chemistry.chemical_classification Reactive oxygen species Dose-Response Relationship Drug General Neuroscience Chloramines Hydrogen Peroxide Oxidants Glutathione Acetylcysteine Phrenic Nerve Synaptic vesicle exocytosis 030104 developmental biology medicine.anatomical_structure chemistry Second messenger system Biophysics Female Synaptic Vesicles Reactive Oxygen Species 030217 neurology & neurosurgery Intracellular |
Zdroj: | Neuroscience. 399:135-145 |
ISSN: | 0306-4522 |
Popis: | Hydrogen peroxide (H2O2) is one of the reactive oxygen species (ROS), endogenously produced during metabolism, which acts as a second messenger. In skeletal muscles, hypoxia- or hyperthermia-induced increase in H2O2 might affect synaptic transmission by targeting the most redox-sensitive presynaptic compartment (Giniatullin et al., 2006). However, the effects of H2O2 as a signal molecule have not previously been studied in different patterns of the synaptic activity. Here, using optical and microelectrode recording of synaptic vesicle exocytosis, we studied the use-dependent action of low concentrations of H2O2 and other oxidants in the mouse neuromuscular junction. We found that: (i) H2O2 at low micromole concentrations inhibited both spontaneous and evoked transmitter releases from the motor nerve terminals in a use-dependent manner, (ii) the antioxidant N-acetylcysteine (NAC) eliminated these depressant effects, (iii) the influence of H2O2 was not associated with lipid oxidation suggesting a pure signaling action, (iv) the intracellular oxidant Chloramine-T or (v) the glutathione depletion produced similar to H2O2 depressant effects. Taken together, our data revealed the effective inhibition of neurotransmitter release by ROS, which was proportional to the intensity of synaptic activity at the neuromuscular junction. The combination of various oxidants suggested an intracellular location for redox-sensitive sites responsible for modulation of the synaptic transmission in the skeletal muscle. |
Databáze: | OpenAIRE |
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