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CHAPTER 4 persist for at least 6 months (Gwak et al., 2012). The increased GFAP expression throughout the cord segment within 24-hours post-injury (Figure 4.7), which persisted for at least 7 days (Figure 4.6), is consistent with this earlier study. Also congruent with previous studies (Hernangomez et al., 2016; Lee-Kubli et al., 2016), are reports of similar GFAP basal levels of 5% or below, in uninjured animals (Figure 4.7). Limited studies have shown the effect of 670 nm treatment following spinal cord injury on astrocyte activation or GFAP upregulation, although similar effects using 810 nm have been documented (Byrnes et al., 2005). Other groups have previously demonstrated a reduction in GFAP expression following light treatment in Müller cells in the retina (Begum et al., 2013; Marco et al., 2013), and a decrease in GFAP expression by 670 nm irradiation in the brain of monkeys with Parkinson’s disease (El Massri et al., 2016). The present study is the first demonstration that astrocytic hypertrophy is reduced by daily 670 nm treatment from 3-dpi following spinal cord injury. The reduced GFAP cannot account for the early (i.e. 1-dpi) red light-induced pain relief, as GFAP expression was not observed at this time. However, it would be interesting to examine GFAP at time points at, and beyond 7-dpi, when pain relief in the hypersensitive population appears to commence. Surprisingly the reduction in GFAP did not appear to arise from the IL1β+ astrocyte subpopulation (Figure 4.8). This is unexpected because IL1β is strongly implicated in the development of hypersensitivity (Calvo et al., 2012). Subpopulations of GFAP+ astrocytes have been reported before and IL1β+ astrocytes are considered to be pro-inflammatory and neurotoxic (Liddelow et al., 2017). However, no other studies may provide clues as to what astrocyte subpopulation was affected by red light in the present study. This is an area requiring further studies. IL1β, produced by both astrocytes and microglia/macrophages, is a cytokine that not only augments inflammation, but also acts on both pre- and post-synaptic terminals to initiate and maintain pain (Calvo et al., 2012; Clark et al., 2015). 670 nm treatment had no effect on IL1β production in microglia/macrophages following spinal cord injury from 1 to 7-dpi (Figure 4.9). This observation is consistent with the previous study (Hu et al., 2016) showing no effect of 670 nm on pro-inflammatory microglia/macrophage (M1), and another study where the authors showed no effect of 810 nm on IL1β expression at either 6-hours post-injury or 4-dpi following spinal cord injury (Byrnes et al., 2005). However, other studies have reported decreases in IL1β expression by light treatment in other injury models (Lee et al., 2016; Sahu et al., 2015). This discrepancy suggests that light treatment may activate different cell pathways in different injury models. As IL1β is a significant player in the regulation of pain, the present study suggests that the pain-alleviating effect of 670 nm light treatment may be independent, or downstream to IL1β, at least up to the first 7 days. There was a significant decrease in UNOS expression, a surrogate marker for iNOS in microglia/macrophages, following 670 nm treatment in spinal cord injured animals (Figure 4.10). Byrnes et al. (2005) found a significant reduction in iNOS transcription that was measured by 107PDF Image | Effects of Red Light Treatment on Spinal Cord Injury
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