摘要
Following trauma to the central nervous system （CNS）, cells in the lesion site die rapidly. In addition, neurons and glia be- yond the initial lesion are vulnerable. These cells can undergo delayed death due to metabolic events that follow the initial trauma, via mechanisms thought to he triggered by gluta- mate-induced excitotoxicity and Ca2＋ overload, leading to mitochondrial dysfunction, associated with increased oxida- tive stress （Camello-Almaraz et al., 2006; Peng and Jou, 2010）. The resultant death of areas of grey and white matter adjacent to the lesion site is termed secondary degeneration, and is a feature of brain and spinal cord injury （Park et al., 2004; Gi- aume et al., 2007）. Secondary degeneration contributes sub- stantially to functional loss following neurotrauma （Profyris et al., 2004; Farkas and Povlishock, 2007） and rescuing this intact, but vulnerable, tissue is considered critical to mini- mising adverse sequelae and improving long term functional outcomes after CNS trauma （Fehlings et al., 2012）. However, our understanding of many of the metabolic events thought to contribute to secondary degeneration is based largely on in vitro studies （Khodorov, 2004; Tretter et al., 2007; Peng and Jou, 2010） and there is a need to confirm the relevance of these mechanisms in vivo, as well as their structural and func- tional consequences.
Following trauma to the central nervous system （CNS）, cells in the lesion site die rapidly. In addition, neurons and glia be- yond the initial lesion are vulnerable. These cells can undergo delayed death due to metabolic events that follow the initial trauma, via mechanisms thought to he triggered by gluta- mate-induced excitotoxicity and Ca2＋ overload, leading to mitochondrial dysfunction, associated with increased oxida- tive stress （Camello-Almaraz et al., 2006; Peng and Jou, 2010）. The resultant death of areas of grey and white matter adjacent to the lesion site is termed secondary degeneration, and is a feature of brain and spinal cord injury （Park et al., 2004; Gi- aume et al., 2007）. Secondary degeneration contributes sub- stantially to functional loss following neurotrauma （Profyris et al., 2004; Farkas and Povlishock, 2007） and rescuing this intact, but vulnerable, tissue is considered critical to mini- mising adverse sequelae and improving long term functional outcomes after CNS trauma （Fehlings et al., 2012）. However, our understanding of many of the metabolic events thought to contribute to secondary degeneration is based largely on in vitro studies （Khodorov, 2004; Tretter et al., 2007; Peng and Jou, 2010） and there is a need to confirm the relevance of these mechanisms in vivo, as well as their structural and func- tional consequences.
基金
support from the Neurotrauma Research Program of Western Australia
funded through the Road Trauma Trust Account, Western Australia
supported by National Health & Medical Research Council of Australia (NHMRC) Project Grant APP1061791
