11C-PK11195 PET for the In Vivo Evaluation of Neuroinflammation in the Rat Brain After Cortical Spreading Depression

Journal of Nuclear Medicine

Miho Shukuri¹  Yasuyoshi Watanabe¹  Yasuhiro Wada¹  Yasuhisa Tamura¹  Hirotaka Onoe¹  Misato Takashima-Hirano¹  Yosky Kataoka¹  Hisashi Doi¹  Tadayuki Takashima¹  Yilong Cui¹ 

关键词: binding potential;    microglia;    peripheral benzodiazepine receptor;    migraine;   

DOI  :  10.2967/jnumed.109.066498

学科分类：医学（综合）

来源: Society of Nuclear Medicine

【 摘 要 】

Neurogenic inflammation triggered by extravasation of plasma protein has been hypothesized as a key factor in the generation of the pain sensation associated with migraine. The principal immune cell that responds to this inflammation is the parenchymal microglia of the central nervous system. Methods: Using a PET technique with 11C-(R)-[1-(2-chlorophenyl)-N-methyl-N-(1-methyl-propyl)-3-isoquinolinecarboxamide] (11C-PK11195), a PET ligand for peripheral type–benzodiazepine receptor, we evaluated the microglial activation in the rat brain after generation of unilateral cortical spreading depression, a stimulation used to bring up an experimental animal model of migraine. Results: We found a significant increase in the brain uptake of 11C-PK11195, which was completely displaceable by the excess amounts of unlabeled ligands, in the ipsilateral hemisphere of the spreading depression–generated rats. Moreover, the binding potential of 11C-PK11195 in the spreading depression–generated rats was significantly higher than that in the sham-operated control rats. Conclusion: These results suggest that as an inflammatory reaction, microglial cells are activated in response to the nociceptive stimuli induced by cortical spreading depression in the rat brain. Therefore, the 11C-PK11195 PET technique could have a potential for diagnostic and therapeutic monitoring of neurologic disorders related to neuroinflammation such as migraine.

【 授权许可】

Unknown