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CHAPTER 3 demonstrated functional improvements of some motor tasks; also consistent with improved locomotor function observed in this study. While the mechanisms for 810 nm vs. 670 nm wavelengths to suppress microglia/macrophage activation and improve motor function cannot be speculated, it is noteworthy that both wavelengths evoke peak levels of cytochrome C oxidase activity and ATP production (Desmet et al., 2006). However, wavelength (i.e. 660 nm vs. 780 nm) has been shown to alter the expression of inflammatory mediators expressed by activated pro- inflammatory microglia/macrophages (Fernandes et al., 2015), and light dosage has been shown to alter the balance of M1/M2 cell expression (von Leden et al., 2013). These in vitro studies suggest that other mechanisms, unrelated to cytochrome C oxidase, may influence the inflammatory microenvironment following light treatment. Furthermore, they highlight the necessity for thorough investigations to establish the therapeutic limits of any wavelength under investigation. While others have demonstrated the impact of wavelength and dose on inflammatory cells in vitro (Fernandes et al., 2015; von Leden et al., 2013), this study is the first to demonstrate the effect of 670 nm light on the polarization of activated microglia/macrophages following spinal cord injury in vivo. The pattern and sequence of pro-inflammatory M1 (CD80+ED1+) cell activation, cell death, followed by anti-inflammatory/wound-healing M2 (Arginase1+ED1+) recruitment observed in sham-treated animals in this study is consistent with what is expected under conditions of spinal cord injury and repair (David and Kroner, 2011; Kigerl et al., 2009). However, the current data indicates that red light-induced reduction of cell death is preceded by the upregulation of M2 cells as early as one day post-injury. This is intriguing because the M2 cell expression preceded that of the M1 cells, indicating that red light drastically altered the normal sequence of inflammatory events. It is therefore speculated that the early presence of protective M2 cells may have caused the reduced subsequent population of dying (TUNEL+) cells. Insufficient expression of the M2 subtype in spinal cord injury, in contrast to peripheral nerve injury, has been suggested to be a contributing factor to the poorer regenerative capacity and functional outcomes in spinal cord injury compared to peripheral nerve injury (David and Kroner, 2011; Kigerl et al., 2009). That red light had a strong impact on promoting the M2 cell types as early as 24 h after treatment followed by reduced levels of cell death and then improved sensory and motor functional outcomes thereafter, is consistent with previous suggestions that enhancing the M2 population during recovery from spinal cord injury may indeed significantly contribute to improving functional outcomes following spinal cord injury (Kigerl et al., 2009). 3.6 Conclusion Modulating the severity of neuropathic pain by simply applying red light is an exciting prospect with great significant clinical relevance, despite not yet fully understanding the mechanism behind photobiomodulation. The current data demonstrates that red light treatment, a non-invasive and cost-effective treatment, is able to significantly reduce the severity of pain in rats acutely after 75PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
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