Mitsumoto Yasuhide, Mori Atsushi, Ohashi Satoshi, Nakai Masami, Moriizumi Tetsuji
Second Institute of New Drug Discovery, Otsuka Pharmaceutical Co., Ltd., Tokushima-city, Tokushima 771-0192, Japan.
Neurosci Res. 2005 Jan;51(1):111-5. doi: 10.1016/j.neures.2004.09.012.
The present study was undertaken to examine whether 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes damage of dopaminergic glomerular cells of the olfactory bulb (OB) in C57BL/6 mice. At 3 days after MPTP treatment, dopamine level in the striatum and the OB decreased to 13% and 84% of the control mice, respectively. While a small reduction of tyrosine hydroxylase protein level was observed in the OB of MPTP-treated mice, dopamine transporter (DAT) was undetectable at the protein level in this region. These results indicate that the DAT protein level could account for resistance of the OB to the Parkinsonism-inducing toxin.
本研究旨在探讨1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）是否会对C57BL/6小鼠嗅球（OB）的多巴胺能肾小球细胞造成损伤。MPTP处理后3天，纹状体和嗅球中的多巴胺水平分别降至对照小鼠的13%和84%。虽然在MPTP处理的小鼠嗅球中观察到酪氨酸羟化酶蛋白水平略有降低，但该区域的蛋白质水平未检测到多巴胺转运体（DAT）。这些结果表明，DAT蛋白水平可能是嗅球对帕金森病诱导毒素具有抗性的原因。
