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Updated: Aug 28, 2025
Author Spotlight: Using Zebrafish to Explore Microglia Migration During Brain Development
Published on: May 17, 2024
Roles of Ca2+ activity in injury-induced migration of microglia in zebrafish in vivo
Tian Du1, Xi Zhou1, Robert Du Yang Zhang2
1Faculty of Art and Science, University of Toronto, 555 University Ave, Toronto, Ontario, M5G 1X8, Canada.
Abstract:
Microglia are the resident immune cells in the brain. It is well known that brain injury can activate the microglia and induce its directional migration towards the injury sites for exerting immune functions. While extracellular ATP released from the injury site mediates the directionality of activated microglia's migration, what endows activated microglia with migration capability remains largely unexplored. In the present study, we used the larval zebrafish as an in vivo model to visualize the dynamics of both morphology and Ca2+ activity of microglia during its migration evoked by local brain injury. We found that, in response to local injury, activated microglia exhibited an immediate Ca2+ transient and later sustained Ca2+ bursts during its migration towards the local injury site. Furthermore, suppression of Ca2+ activities significantly retarded microglial cell migration. Thus, our study suggests that intracellular Ca2+ activity is required for activated microglia's migration.
Insights
Brain injury activates microglia, but their migration ability is unknown. This study shows intracellular calcium activity is essential for microglia migration towards brain injury sites.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are brain's immune cells, activated by injury.
- They migrate directionally to injury sites, guided by extracellular ATP.
- The mechanism enabling microglial migration capability is largely unknown.
Purpose of the Study:
- To investigate the role of intracellular calcium (Ca2+) activity in microglial migration following brain injury.
- To visualize microglial dynamics, including morphology and Ca2+ activity, during migration in a live model.
Main Methods:
- Utilized larval zebrafish as an in vivo model.
- Observed microglia morphology and Ca2+ activity dynamics using live imaging.
- Induced local brain injury to evoke microglial response.
- Manipulated Ca2+ activity to assess its effect on migration.
Main Results:
- Activated microglia showed immediate Ca2+ transients and sustained Ca2+ bursts during migration.
- Suppression of Ca2+ activity significantly slowed microglial cell migration.
- Larval zebrafish model allowed real-time visualization of microglial behavior.
Conclusions:
- Intracellular Ca2+ activity is a critical requirement for activated microglia migration towards brain injury.
- This finding sheds light on the cellular mechanisms underlying neuroinflammation and brain repair.
