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The Journal of Neuroscience, March 15, 2006, 26(11):3045-3055; doi:10.1523/JNEUROSCI.5200-05.2006

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Development/Plasticity/Repair
Spatial Heterogeneity in Oligodendrocyte Lineage Maturation and Not Cerebral Blood Flow Predicts Fetal Ovine Periventricular White Matter Injury

Art Riddle,¹ Ning Ling Luo,¹ Mario Manese,¹ Douglas J. Beardsley,¹ Lisa Green,⁴ Dawn A. Rorvik,⁴ Katherine A. Kelly,⁴ Clyde H. Barlow,⁴ Jeffrey J. Kelly,⁴ A. Roger Hohimer,³ and Stephen A. Back^1,2

Departments of ¹Pediatrics, ²Neurology, and ³Obstetrics and Gynecology, Oregon Health and Science University, Portland, Oregon 97239-3098, and ⁴Barlow Scientific, Inc., and The Evergreen State College, Olympia, Washington 95805

Correspondence should be addressed to Dr. Stephen A. Back, Department of Pediatrics, Hatfield Research Center, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239-3098. Email: Backs{at}ohsu.edu

Although periventricular white matter injury (PWMI) is the leading cause of chronic neurological disability and cerebral palsy in survivors of premature birth, the cellular-molecular mechanisms by which ischemia-reperfusion contributes to the pathogenesis of PWMI are not well defined. To define pathophysiologic relationships among ischemia, acute cerebral white matter damage, and vulnerable target populations, we used a global cerebral ischemia-reperfusion model in the instrumented 0.65 gestation fetal sheep. We developed a novel method to make repeated measurements of cerebral blood flow using fluorescently labeled microspheres to resolve the spatial heterogeneity of flow in situ in three-dimensional space. Basal flow in the periventricular white matter (PVWM) was significantly lower than in the cerebral cortex. During global cerebral ischemia induced by carotid occlusion, flow to all regions was reduced by nearly 90%. Ischemia of 30 or 37 min duration generated selective graded injury to frontal and parietal PVWM, two regions of predilection for human PWMI. Injury was proportional to the duration of ischemia and increased markedly with 45 min of ischemia to extensively damage cortical and subcortical gray matter. Surprisingly, the distribution of PVWM damage was not uniform and not explained by heterogeneity in the degree of white matter ischemia. Rather, the extent of white matter damage coincided with the presence of a susceptible population of late oligodendrocyte progenitors. These data support that although ischemia is necessary to generate PWMI, the presence of susceptible populations of oligodendrocyte progenitors underlies regional predilection to injury.

Key words: blood flow; cerebral blood flow; hypoxia-ischemia; white matter; neonatal prenatal; oligodendrocyte; periventricular; ischemia; injury; development; blood–brain

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Received May 4, 2005; revised Jan. 23, 2006; accepted Jan. 24, 2006.

Correspondence should be addressed to Dr. Stephen A. Back, Department of Pediatrics, Hatfield Research Center, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239-3098. Email: Backs{at}ohsu.edu

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