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CHAPTER 1 cavity acting as a physical barrier for the regenerating axons. Chondroitin sulphate proteoglycan, heavily involved in glial scar formation (Fawcett and Asher, 1999), is believed to inhibit axonal sprouting (Zuo et al., 1998); therefore, providing a chemical barrier for regeneration. However, not all parts of gliosis and scar formation are detrimental. Depletion of astrocytes leads to increased inflammation, failure of vasculature repair, worsened functional recovery (Faulkner et al., 2004; Okada et al., 2006). These studies suggest an essential role of astrocytes and gliosis in the pathophysiology of spinal cord injury. A controlled gliosis and cavity formation would be beneficial to the recovery. Cell death Cell death following spinal cord injury occurs through various processes. The first cause is the disruption of the cell membrane, either through direct mechanical insult or lipid peroxidation. Cells, especially neurons and neuroglia, also die from excitotoxicity due to the excessive Ca2+ influx (Simon et al., 2009; Xiong et al., 2007). Excessive Ca2+ triggers a cascade of events, including the activation of calpain and caspase. These two enzymes then degrade membranes, cytoskeletons and nuclear substrates (Ray et al., 2003). Energy depletion due to hypoxia and mitochondrial dysfunction from ROS and RNS also cause cell death. Decreased production of ATP leads to the dysfunction of ion channels and therefore exaggerates Ca2+-triggered cell death (Boutilier, 2001). In addition, inflammatory cells also contribute to cell death through their secretions, and therefore, inducing apoptosis (Shuman et al., 1997). Apart from local cell death, neurons and oligodendrocytes distal to the injury epicentre are also subjected to death due to severing of axons and/or degeneration of myelin (Casha et al., 2001). Wallerian degeneration and demyelination Primary damage to the spinal cord results in the severing of axons, loss of myelination, loss of neurons and loss of oligodendrocytes at the injury epicentre. Loss of oligodendrocytes at the injury epicentre leads to further demyelination. Demyelination poses two main detrimental effects depending on the time frame. Acutely, it slows down conduction along the nerve fibres leading to delays or conduction block (Hall and Traystman, 2009; McTigue, 2008). In the long term, axons, without the protection of myelin, are more susceptible to degeneration, which ultimately leads to more neuronal loss (Oyinbo, 2011). In vivo imaging showed both proximal and distal axonal degeneration (hundreds of μm) 30 min following spinal cord injury, and this degeneration is similar to the delayed Wallerian degeneration in distal disconnected axons (Kerschensteiner et al., 2005). This ongoing degeneration and demyelination might be due to apoptosis (Crowe et al., 1997). Therefore, therapies that target cell death may weaken or even stall degeneration and demyelination. 6PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
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