Enhanced Oligodendrocyte Survival after Spinal Cord Injury in Bax-Deficient Mice and Mice with Delayed Wallerian Degeneration

• DOI: 10.1523/jneurosci.23-25-08682.2003
• Publication Date: 2018-04-12T23:25:04Z
• Authors: Hongxin Dong; Alicia Fazzaro; Chuanxi Xiang; Stanley J. Korsmeyer; Mark F. Jacquin; John W. McDonald
• Keywords: Wallerian degeneration

Mechanisms of oligodendrocyte death after spinal cord injury (SCI) were evaluated by T9 level hemisection in wild-type mice (C57BL/6J and Bax+/+ mice), Wlds which severed axons remain viable for 2 weeks, deficient the proapoptotic protein Bax (Bax-/-). In lateral white-matter tracts, substantial was evident ipsilateral white matter 3-7 mm rostral caudal to site 8 d injury. Ultrastructural analysis expression anti-activated caspase-3 characterized ongoing at as primarily apoptotic. Oligodendrocytes selectively preserved compared with C57BL/6J injury, when remained verified antereograde labeling vestibular tract. However, 30 animals already degenerated, oligodendrocytes lost, numbers then equivalent control mice. contrast, prevented both time points Bax-/- When cultured exposed staurosporine or cyclosporin A, drugs known stimulate apoptosis oligodendrocytes, those from but not Bax+/- resistant apoptotic death. three groups equally vulnerable excitotoxic necrosis induced kainate. On basis these data, we hypothesize that Wallerian degeneration follows SCI removes axonal support induces triggering expression.