@misc{oai:repo.qst.go.jp:00068886,
 author = {Ki, Hin and Higuchi, Makoto and Maeda, Jun and Inaji, Motoki and Okauchi, Takashi and Zhang, Ming-Rong and Suzuki, Kazutoshi and Andou, Kiyoshi and Suhara, Tetsuya and 季 斌 and 樋口 真人 and 前田 純 and 稲次 基希 and 岡内 隆 and 張 明栄 and 鈴木 和年 and 安東 潔 and 須原 哲也},
 month = {Dec},
 note = {The present study was aimed at clarifying correlation between signature of gliosis and type of neuronal insult, by analyzing glial activation in neurotoxicant-induced neurodegeneration including methamphetamine (METH), 6-hydoxydomaine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), kainic acid (KA), and cuprizone. Analyses using tracers for in vivo imaging along with immunohistochemistry revealed that METH, 6-OHDA, and MPTP induced serious loss of dopaminergic terminals and pronounced astrogliosis in the striatum of mouse, rat, and marmoset, respectively, while morphology and number of microglia as well as levels of peripheral-type benzodiazepine receptor/recognition site (PBR) were not altered in the same regions. Cuprizone and KA induced a notable increase in PBR levels in the striatum, hippocampus, entorhinal cortex and striatum-nigra, and this alteration was colocalized with severe demyelination. Additional histopathological analyses illustrated a tight correlation of demyelination with significant microgliosis and increased PBR levels, while degeneration of dopaminergic neuron, which is know to project unmyelinated axons, was concomitant with notable astrogliosis and barely detectable microgliosis. These findings delineate two distinct triggers of glial activation, one inducing both astroglial and microglial responses in close association with demyelination and the other being exclusively accompanied with augmented astroglial activity., 第21回日本薬物動態学会年会},
 title = {Distinct glial responses to diverse chemical neurotoxicants in the striatum as monitored by imaging agents},
 year = {2006}
}