Journal
THERAPEUTIC HYPOTHERMIA AND TEMPERATURE MANAGEMENT
Volume 1, Issue 1, Pages -Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ther.2010.0011
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Funding
- [NS030291]
- [NS042133]
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The purpose of this study was to document patterns of oligodendrocyte vulnerability to traumatic brain injury (TBI) and determine whether post-traumatic hypothermia prevents oligodendrocyte cell loss. Sprague-Dawley rats underwent moderate fluid percussion brain injury. Thirty minutes after TBI, brain temperature was reduced to 33 degrees C for 4 hours or maintained at normothermic levels (37 degrees C). Animals were perfusion-fixed for quantitative immunohistochemical analysis at 3 (n = 9) or 7 (n = 9) days post-TBI. Within the cerebral cortex, external capsule, and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes at 3 and 7 days following TBI were significantly decreased compared with sham-operated rats (p < 0.02). Double-labeling studies showed that vulnerable oligodendrocytes expressed increased Caspase 3 activation compared with sham. Post-traumatic hypothermia significantly reduced the number of CC1-positive oligodendrocytes lost after normothermia TBI in white matter tracts (p < 0.01). This model of TBI leads to quantifiable regional patterns of oligodendrocyte vulnerability. Post-traumatic hypothermia protects oligodendrocytes by interfering with Caspase 3-mediated cell death mechanisms. Therapeutic hypothermia may improve functional outcome by attenuating trauma-induced oligodendrocyte cell death, subsequent demyelination, and circuit dysfunction.
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