Abstract
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°C for 4 hours or maintained at normothermic levels (37°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.
