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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathophysiology

Background:

  • Cortical spreading depolarizations (CSDs) are waves of neuronal activity linked to migraine and brain injury.
  • CSDs are known to disrupt the blood-brain barrier (BBB), but the underlying mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the mechanisms of CSD-induced BBB disruption.
  • To investigate the role of endothelial transcytosis, tight junctions, pericytes, and specific molecular pathways in CSD-mediated BBB breakdown.

Main Methods:

  • Evoked CSDs in mice using KCl or optogenetics.
  • Assessed BBB disruption via Evans blue and dextran extravasation.
  • Examined endothelial cell ultrastructure using transmission electron microscopy.
  • Investigated the effects of ROCK inhibitors (fasudil, KD025) and hyperoxia.

Main Results:

  • CSD-induced BBB opening is mediated by increased endothelial transcytosis, beginning 3-6 hours post-CSD and lasting ~24 hours.
  • Endothelial tight junctions, pericytes, and basement membrane integrity were preserved.
  • BBB disruption was exclusively dependent on caveolin-1 and required ROCK2 activity.
  • Hyperoxia did not prevent BBB breakdown, indicating independence from tissue hypoxia.

Conclusions:

  • CSDs cause transient BBB disruption primarily through caveolin-1-dependent transcytosis.
  • ROCK2 activity is crucial for CSD-induced BBB breakdown.
  • Findings provide mechanistic insights into BBB dysfunction following CSDs, relevant for neurological disorders.