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Mitochondrial ROS modulate presynaptic plasticity in the drosophila neuromuscular junction
Irina Stavrovskaya1, Bethany Kristi Morin1, Stephen Madamba1
1Baruch College and CUNY Graduate Center, 1 Baruch Way, New York, NY, 10010, USA.
Redox Biology
|December 25, 2024
Summary
Mitochondrial reactive oxygen species (ROS) can enhance synaptic potentiation and presynaptic function. This study reveals a novel signaling role for mitochondrial ROS in neuronal communication and plasticity.
Area of Science:
- Neuroscience
- Cell Biology
- Mitochondrial Biology
Background:
- Elevated mitochondrial reactive oxygen species (ROS) are linked to neurodegenerative diseases.
- The role of mitochondrial ROS in normal presynaptic function and plasticity is understudied.
Purpose of the Study:
- Investigate the role of mitochondrial ROS in presynaptic function and short-term plasticity.
- Explore the molecular mechanisms underlying mitochondrial ROS signaling at the synapse.
Main Methods:
- Utilized optogenetics to induce ROS emission in presynaptic mitochondria.
- Performed whole-cell electrophysiological recordings and live confocal imaging in Drosophila melanogaster.
- Measured synaptic potentiation via spontaneous mini excitatory junction potentials and active zone marker expression.
Main Results:
- Optogenetic induction of mitochondrial ROS emission led to synaptic potentiation.
- This effect was blocked by catalase, indicating a role for hydrogen peroxide (H2O2).
- Increased active zone marker Brp/Erc1 suggests redox modulation of vesicle release sites.
Conclusions:
- Mitochondrial ROS signaling plays a novel role in presynaptic function and plasticity.
- Redox switches in active zone components are potential targets of mitochondrial H2O2.
- Findings provide insights into redox-based mechanisms of neuronal communication.
