Ghrelin regulates long-chain fatty CoAs and ROS in the midbrain. A , Individual LCFA CoAs measured 3 h after ghrelin injection (10 nmol, i.p.). ^aSignificant with respect to saline controls. B , Quantification of ROS in TH neurons of the SNpc using dihydroethidium (DHE) shows that ghrelin reduces TH ROS production in UCP2 wt mice but robustly increases ROS in ucp2−/− mice. This suggests that the inability of ghrelin to enhance UCP2 in ucp2−/− mice prevents the buffering of increased ROS produced by increased fatty acid oxidation. Data are presented as the mean ± SEM. ^aSignificant with respect to saline wt controls; ^b,csignificant with respect to saline UCP2 wt and −/−, respectively (n = 5, p < 0.05). C1 , C2 , Representative images showing dual-channel ROS production (red) in TH neurons (green) of the SNpc in saline- and ghrelin-treated UCP2 wt mice. D1 , D2 , Representative images showing single-channel ROS production in saline- and ghrelin-treated UCP2 wt mice. E1 , E2 , Representative images showing dual-channel ROS production (red) in TH neurons (green) of the SNpc in saline- and ghrelin-treated ucp2−/− mice. F1 , F2 , Representative images showing single-channel ROS production in saline- and ghrelin-treated ucp2−/− mice. Data are presented as the mean ± SEM. Scale bar (in E2 ) C–F , 10 μm.