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Action of Hydrogen Peroxide on Synaptic Transmission at the Mouse Neuromuscular Junction.

Abstract：

: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.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Giniatullin A,Petrov A,Giniatullin R

doi

10.1016/j.neuroscience.2018.12.027

subject

Has Abstract

pub_date

2019-02-10 00:00:00

pages

135-145

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(18)30843-1

journal_volume

399

pub_type

杂志文章

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