A) Using micro-PET and selective radioactive tracers we measured in vivo the extent of dopamine terminal loss and inflammatory response 12 (top panel) and 21 (bottom panel) days after the 6-OHDA lesion. Color-coded images of 11C-CFT ((2β-carbomethoxy-3β-(4-fluorophenyl) tropane, a dopamine transporter ligand) and 11C-PK11195 (a peripheral-type benzodiazepine ligand that binds to microglia) in a representative animal of each group. As reported in our previous study  6-OHDA injection resulted in a marked decrease of 11C-CFT binding in the striatum and a parallel increase in 11C PK-11195 binding in the control (vehicle) group. The increase in 11C PK 11195 binding was absent in COXIB treated animals and in both groups at 21 days post lesion. B-C) Microphotographs of TH fiber density in the striatum in representative animals (same as shown in A). D) Volumetric analysis of fiber loss in the lesioned striatum showed a marked reduction at 12 days, that partially recovered at 21 days post-lesion (*, p < 0.01). TH striatal volumes were significantly larger in COXIB treated than in the vehicle group (#, p < 0.01). E) At 12 days post-lesion, both treatment groups displayed a ~40% loss of TH positive cell bodies in the SN. The progressive loss of DA cell bodies between 12 and 21 days post-lesion in the vehicle treated rats was significant (* p< 0.01) while there was no significant difference in DA cell bodies in the COXIB treated rats between 12 and 21 days. At 21 days the DA cell loss in the SN was significantly higher in vehicle treated animals (#, p < 0.05). Scale bar: 30 μm.