Fig. 3

Partial sciatic nerve ligation induces persistent mitochondrial dysfunction in injured nerves. a The proportion of the oxygen consumption rate specific to mitochondrial ATP production is persistently reduced following partial sciatic nerve ligation, demonstrating dysfunction in mitochondrial ATP production. b Additionally, the mitochondria of injured nerves have no spare capacity. When stimulated pharmacologically with a proton uncoupling agent, mitochondria are unable to consume any more oxygen after nerve injury. This suggests that the mitochondria in injured nerves are under bioenergetic stress and are already operating at their maximum capabilities for ATP production. c Maximal mitochondrial respiration is persistently reduced following nerve injury. This demonstrates that nerve injury reduces the ability of mitochondria to perform oxidative processes. d Futile proton cycling, or proton leak, is increased in mitochondria following nerve injury. Mitochondria undergo changes to allow more protons to passively dissipate the proton motive force after nerve injury. This avails fewer protons for ATP synthesis