Open AccessOligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia
Author(s) -
George Lotocki,
Juan Pablo de Rivero Vaccari,
Ofelia F. Alonso,
Juliana Sanchez Molano,
Ryan Nixon,
W. Dalton Dietrich,
Helen M. Bramlett
Publication year - 2011
Publication title -
therapeutic hypothermia and temperature management
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.323
H-Index - 12
eISSN - 2153-7933
pISSN - 2153-7658
DOI - 10.1089/ther.2010.0011
Subject(s) - traumatic brain injury , hypothermia , medicine , oligodendrocyte , white matter , corpus callosum , anesthesia , internal capsule , pathology , central nervous system , magnetic resonance imaging , myelin , psychiatry , radiology
The purpose of this study was to document patterns of oligodendrocyte vulnerability to TBI and determine whether posttraumatic 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 hrs 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 to sham operated rats (p<0.02). Double-labeling studies showed that vulnerable oligodendrocytes expressed increased Caspase 3 activation compared to sham. Posttraumatic 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. Posttraumatic 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.