抄録
During oligodendrocyte lineage progression, selective vulnerability of late oligodendrocyte progenitors (preOLs) to hypoxia-ischemia (H-I) are shown, giving probable etiology of periventricular leukomalacia (PVL), selective white matter damage of human premature infant. In rats, preOLs are mainly detected at postnatal day 2 (P2)-P4. However, H-I rodent models for PVL were made mainly at P7 until now. To investigate whether H-I to preOLs in P2-P4 rats produces more similar pathological changes of PVL (coagulation necrosis, increase microglia, vacuolation of white matter), right common carotid artery in Wistar rats (P2-P4) was occluded (RCAO) followed by various concentration of oxygen (6-8%) with various time (0-90 mins). We found that H-I by RCAO followed by 6% oxygen for 60 min caused high death rates: 64% in P2, 50% in P3, 89% in P4 pups. No histological change was shown in Hematoxilin-Eosin (HE) staining in P2 rats at 2 days after H-I. Typical histological changes of PVL were shown in P3 rats survived: partial collapse of layer formation in cortex, and appearance of ED-1 positive cells. Data suggest that RCAO with 6% hypoxia for 60 min in P3 pups induced more similar pathological changes of PVL in rats, supporting that specific vulnerability of preOLs to H-I in vivo would, at least in part, explain the etiology of PVL. [Jpn J Physiol 55 Suppl:S236 (2005)]
