✓Establish unilateral carotid ligation and hypoxia protocols in P6 mice
✓Induce periventricular white matter lesions with/without LPS injection
✓Evaluate PVL-like brain injury outcomes in neonatal mouse models
✓Assess hypoxia/ischemia and infection contributions to premature brain injury
Protocol
Biopharma Insights We established mouse models of periventricular leukomalacia (PVL), the predominant brain injury in premature infants characterized by periventricular white matter lesions. Hypoxia/ischemia with/without systemic infection are the primary causes of PVL. Unilateral carotid ligation and hypoxia exposure with/without lipopolysaccharide injection creates PVL-like lesions in P6 mice.
Difficulty
advanced
Total time
~45 min/mouse (acute induction); 3–7 days (outcome assessment post-injury)
Model organism
Mouse (P6 neonatal, mixed background implied)
Biosafety
BSL-2
Steps
1
Understand PVL pathophysiology and model rationale
Review periventricular leukomalacia as the predominant white matter injury in premature infants and the dual roles of hypoxia/ischemia and systemic infection in disease etiology.
▶ 00:35
2
Perform unilateral carotid ligation and hypoxia exposure
Ligate the right common carotid artery in P6 mice, then expose animals to hypoxic conditions (with or without prior lipopolysaccharide injection) to induce periventricular white matter lesions.
▶ 01:52
3
Assess resulting PVL-like lesion characteristics
Document the location, extent, and morphology of induced periventricular white matter lesions in ischemic and hypoxic conditions, with or without systemic infection markers.
▶ 03:33
4
Interpret model utility for PVL research
Summarize how the unilateral carotid ligation/hypoxia ± LPS model recapitulates human PVL pathology and informs neuroprotection and therapeutic strategy development.
▶ 05:40
💬 Comments coming soon
New protocols and pitfalls, in your inbox
A short email when we add notable lab videos and failure cases. No spam, unsubscribe anytime.