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Figure 1 | BMC Genomics

Figure 1

From: Comparative analysis of the time-dependent functional and molecular changes in spinal cord degeneration induced by the G93A SOD1 gene mutation and by mechanical compression

Figure 1

Graphs illustrating the profiles of functional, behavioural and weight changes recorded in the models of trauma and genetically-induced spinal cord degeneration employed in this study. The functional and behavioural analyses include the open-field locomotor assessment (BBB score) of rats after mild spinal cord compression and the evaluation of immobility time and rearing episodes in G93A SOD1 mutant rats. For comparison, we report previously published data generated from similar experimental platforms (data taken from Jokic et al. 2007 and Huang et al. 2007) [16, 18]. A1A2: Schematic representation of the average immobility time (A2) and average number of rearing episodes (A1) observed in 4 G93A SOD1 mutant rats with subtle signs of hindlimb paralysis at disease presentation and in 4 wild type rats. Determinations by independent observers were performed at onset and at end-stage disease, based on 2 subsequent 3-minutes video clips recorded during disease development in the 4 G93A SOD1 mutant rats and in the WT littermates. Data previously reported by Jokic et al. [16]. At disease onset, the duration of average immobility time in the wild-type and in the G93A SOD1 mutant animals was similar, whereas a significant increase in duration of immobility time was observed in the G93A SOD1 mutant animals at end stage disease (A2; p < 0.05, ANOVA). A remarkable reduction of rearing episodes is seen in G93A SOD1 mutant rats at end-stage disease (A1; p < 0.001, ANOVA). Disease onset (appearance of first signs of paralysis): 129 +/- 17.3 days. End-stage disease (25–30% loss of body weight): 139 +/- 17 days. B: Individual body weight measurements of 12 G93A SOD1 mutant rats and of 12 age-matched wild type animals from a pre-symptomatic stage to end-stage disease (G93A SOD1 mutant rats presented with either hindlimb or forelimb paralysis at disease onset). The data presented include previous observations obtained from a group of 4 G93A SOD1 mutant rats and 4 wild type rats [16]. The maximum body weight recorded for each G93A SOD1 mutant rat was set at 100% as base-line. The graph indicates body weight measurements performed after this point (the measurements started at 7 weeks of age and were performed every two days), expressed as percentage of the maximum body weight. Disease onset (T0) is indicated at the time of the appearance of the first signs of paralysis (on average at 129 +/- 17.3 days of age). At disease onset, weight loss has been progressing for at least 6 days to a 10 to 15% reduction from maximum body weight. The end-stage disease was set at 25–30% of weight loss (139 +/- 17 days of age in the G93A SOD1 mutants). Weight measurements are expressed as averages of weight determinations of the number of surviving animals reported in the graph (those rats reaching a 25–30% body weight reduction were sacrificed). The graph reports the numbers of surviving animals at each time point. C: the graph illustrates the functional recovery of wild-type female rats after spinal cord compression, measured at 30 minutes, 4 hours, 24 hours and 7 days from mild injury (35 g weight spinal cord compression) using the Basso, Beattie, and Bresnahan (BBB) open-field locomotor assessment. The BBB scoring for each 5 animals right and left hindlimb was graded at the defined time points by two independent blinded observers (red colour code). Also plotted are the BBB scores of Sprague-Dawley rats after a 50 g compression injury (blue colour code, n: 5), taken from previously reported data [18].

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