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Microglial Calcium Waves During the Hyperacute Phase of Ischemic Stroke
Lei Liu1, Kathryn N Kearns1, Ilyas Eli2
1Department of Neurological Surgery (L.L., K.N.K., K.A. Sharifi, S.S., K.W.S., M.Y.S.K., M.P., P.T.), University of Virginia Health System, Charlottesville.
Stroke
|November 9, 2020
Summary
Microglia exhibit calcium activity during ischemic stroke, contributing to brain injury. This activity, linked to cortical spreading depolarizations (CSD), is modulated by inflammation and CRAC channels, offering potential therapeutic targets.
Area of Science:
- Neuroscience
- Cellular Biology
- Pathology
Background:
- Ischemic stroke causes brain injury via pathological responses like cortical spreading depolarizations (CSD).
- Microglia are implicated in CSD propagation, but their intracellular responses during stroke remain unclear.
Purpose of the Study:
- Investigate intracellular calcium activity in microglia during ischemic stroke.
- Determine the role of microglial calcium signaling in CSD and potential therapeutic targets.
Main Methods:
- Utilized a murine stroke model (middle cerebral artery occlusion) with a Cre-dependent GCaMP5/tdTomato reporter.
- Employed high-speed 2-photon microscopy in vivo to record microglial calcium activity.
- Applied inflammatory stimuli and pharmacological inhibitors (CM-EX-137) to modulate responses.
Main Results:
- Observed periodical microglial calcium activity during the hyperacute phase of ischemic stroke.
- Calcium transient frequency peaked early, while amplitudes increased later.
- CSD-like calcium transients were triggered by KCl, enhanced by inflammation, and partially mediated by CRAC channels.
Conclusions:
- Microglia engage in previously unrecognized mechanisms during ischemic brain injury.
- Microglial calcium signaling during CSD presents novel therapeutic intervention possibilities.
