Oligodendrocyte vulnerability following traumatic brain injury in rats

George Lotocki, Juan de Rivero Vaccari, Ofelia Alonso, Juliana Sanchez Molano, Ryan Nixon, Padideh Safavi, W. Dalton Dietrich, Helen M. Bramlett

Research output: Contribution to journalComment/debatepeer-review

61 Scopus citations


Experimental and clinical findings demonstrate that traumatic brain injury (TBI) results in injury to both gray and white matter structures. The purpose of this study was to document patterns of oligodendrocyte vulnerability to TBI. Sprague Dawley rats underwent sham operated procedures or moderate fluid percussion brain injury. Quantitative immunohistochemical analysis was performed on animals perfusion-fixed at 3 (n= 9) or 7 (n= 9) days post-surgery. Within the ipsilateral external capsule and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes were significantly decreased at 3 or 7 days post-TBI compared to sham rats (p< 0.03). At both posttraumatic survival periods, double-labeling studies indicated that oligodendrocytes showed increased Caspase 3 activation compared to sham. These data demonstrate regional patterns of oligodendrocyte vulnerability after TBI and that oligodendrocyte cell loss may be due to Caspase 3-mediated cell death mechanisms. Further studies are needed to test therapeutic interventions that prevent trauma-induced oligodendrocyte cell death, subsequent demyelination and circuit dysfunction.

Original languageEnglish (US)
Pages (from-to)143-148
Number of pages6
JournalNeuroscience Letters
Issue number3
StatePublished - Jul 25 2011


  • Apoptosis
  • Brain trauma
  • Myelin
  • Oligodendrocyte

ASJC Scopus subject areas

  • Neuroscience(all)


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