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Mitochondrial ROS cause motor deficits induced by synaptic inactivity: Implications for synapse pruning
Eva Sidlauskaite1, Jack W Gibson1, Ian L Megson2
1School of Science Engineering and Technology, Abertay University, Dundee DD1 1HG, UK.
Redox Biology
|March 28, 2018
Summary
Mitochondrial reactive oxygen species (ROS) act as sentinels during synapse pruning. Blocking ROS with antioxidants reduced motor deficits caused by synaptic inactivity in tadpoles.
Area of Science:
- Neuroscience
- Developmental Biology
- Cellular Biology
Background:
- Synapse pruning is crucial for refining neural connections during development.
- Mitochondrial reactive oxygen species (ROS) are implicated in cellular processes, but their role in synapse pruning remains unclear.
Purpose of the Study:
- To investigate whether mitochondrial ROS regulate synapse pruning at the neuromuscular junction (NMJ).
- To determine if blocking mitochondrial ROS can ameliorate motor deficits associated with synaptic inactivity.
Main Methods:
- Induced synaptic inactivity at the NMJ in Xenopus laevis tadpoles using neurotoxins and an endogenous pruning cue.
- Measured mitochondrial ROS levels and motor function.
- Administered manganese porphyrin antioxidants (MnTE-2-PyP5+ and MnTnBuOE-2-PyP5+) and a mitochondria-targeted ROS inducer (MitoPQ).
Main Results:
- Synaptic inactivity significantly increased mitochondrial ROS production in vivo.
- Antioxidants MnTE-2-PyP5+ and MnTnBuOE-2-PyP5+ reduced motor deficits induced by synaptic inactivity.
- MitoPQ recapitulated motor deficits, which were rescued by MnTnBuOE-2-PyP5+, confirming mitochondrial ROS's role.
Conclusions:
- Mitochondrial ROS function as sentinels of synaptic activity.
- These findings reveal a novel mechanism by which mitochondrial ROS regulate the consequences of synaptic inactivity during NMJ pruning.
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