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First published online October 16, 2009, 10.2967/jnumed.109.066498
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Journal of Nuclear Medicine Vol. 50 No. 11 1904-1911
© 2009 by Society of Nuclear Medicine
doi: 10.2967/jnumed.109.066498

Basic Science Investigation

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

Yilong Cui1, Tadayuki Takashima2, Misato Takashima-Hirano3, Yasuhiro Wada2, Miho Shukuri4, Yasuhisa Tamura1, Hisashi Doi3, Hirotaka Onoe4, Yosky Kataoka1 and Yasuyoshi Watanabe2

1 Cellular Function Imaging Laboratory, RIKEN Center for Molecular Imaging Science, Kobe, Hyogo, Japan; 2 Molecular Probe Dynamics Laboratory, RIKEN Center for Molecular Imaging Science, Kobe, Hyogo, Japan; 3 Molecular Imaging Labeling Chemistry Laboratory, RIKEN Center for Molecular Imaging Science, Kobe, Hyogo, Japan; and 4 Functional Probe Research Laboratories, RIKEN Center for Molecular Imaging Science, Kobe, Hyogo, Japan

Correspondence: Correspondence or reprints contact: Yilong Cui, Cellular Function Imaging Laboratory, RIKEN Center for Molecular Imaging Science, 6-7-3 Minatojima Minamimachi, Chuo-ku, Kobe, Hyogo 650-007, Japan. E-mail: cuiyl{at}riken.jp

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.

Key Words: binding potential • microglia • peripheral benzodiazepine receptor • migraine

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.


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