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. 2019 Jun 18;10:635. doi: 10.3389/fneur.2019.00635

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Copyright © 2019 Martin, Wong and Hanaford.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mitochondrial oxidative metabolism is amplified acutely in mutant A53T-αSyn after neonatal cortical contusion injury (CCI). (A) Cytochrome c oxidase (COX) enzyme histochemistry showing the in situ enzyme activity of COX in neonatal mouse brain at 24 h after injury at postnatal day 7. The ventrobasal complex of thalamus (VBC), subthalamic nucleus (STN), and hippocampus (Hippo) show intense mitochondrial activation ipsilaterally after CCI. The mediodorsal thalamic nucleus (MD) and hypothalamus (Hypo) are unchanged and similar on both hemispheres. Scale bar = 255 μm. (B) Densitometry measurements of COX enzyme activity reaction product in sham and CCI mice. Values are mean ± SD (n = 10 mice/group). ^*p < 0.05 compared to non-Tg sham; ^**p < 0.01, or ^***p < 0.001 compared to A53T-sham.