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. Author manuscript; available in PMC: 2015 Jul 1.
Published in final edited form as: Exp Neurol. 2014 May 5;257:95–105. doi: 10.1016/j.expneurol.2014.04.026

Fig. 1.

Fig. 1

Effects of NACA treatment on mitochondrial Oxygen Consumption Rate (OCR) following contusion SCI. Comparisons of the OCR in terms of nmol oxygen/min for (A) total (mixed population of synaptic and non-synaptic, (B) synaptic and (C) non-synaptic mitochondria that were assessed 24 hrs post-injury. 5μg mitochondrial protein was used for each sample. SCI significantly decreases ADP phosphorylation rate (State III) and State V-complex I (complex I- driven maximum electron transport) in all three population of mitochondria compared to Naïve (Panels A–C). Compared to Vehicle, treatment with NACA at 75, 150 or 300 mg/kg i.p. significantly maintained respiration for total mitochondria, in a dose-dependent manner (Panel A). For synaptic and non-synaptic mitochondria only 300mg/kg NACA significantly increase mitochondrial OCR compared to Vehicle (Panels B & C, respectively). Bars are group means ± SEM, n=4/group. *p<0.05 compared to Naïve; #p<0.05 compared to Vehicle.