Multiparametric assessment of acute and subacute ischemic neuronal damage: A small animal positron emission tomography study with rat photochemically induced thrombosis model

We evaluated sequential changes in rat brain function up to 14 days after focal ischemic insult with a small animal positron emission tomography (PET). Unilateral focal ischemic cerebral damage was induced by left middle cerebral artery occlusion with a photochemically induced thrombosis (PIT) method. PET scans were conducted with [11C](R)‐PK11195 ([11C](R)‐PK) for peripheral benzodiazepine receptor (PBR), [11C]flumazenil ([11C]FMZ) for central benzodiazepine receptor (CBR), and [18F]fluoro‐2‐deoxy‐D‐glucose ([18F]FDG) for glucose metabolism at before (as “Normal”) and after PIT. At 1 and 3 days after PIT, [18F]FDG indicated lower uptake in the infarct area. Interestingly, unexpectedly high‐[18F]FDG uptake was observed in the peri‐infarct area surrounding the infarct area at day 7. The high‐[18F]FDG uptake region completely overlapped with the high‐[11C](R)‐PK uptake region at day 7, which resulted in the underestimation of neuronal damage. Immunohistochemical data also suggested that the high‐[18F]FDG uptake peak at day 7 was caused by inflammation including microglial cell activation. In contrast, imaging with [11C]FMZ indicated cortical neuronal damage on days 7 and 14 without any disturbance by microglial formation. These results indicated that [18F]FDG might not be a suitable ligand for ischemic neuronal damage detection from acute to subacute phases. Synapse, 2010. © 2010 Wiley‐Liss, Inc.