Boatell M L, Mahy N, Cardozo A, Ambrosio S, Tolosa E, Cruz-Sánchez F F
Neurological Tissue Bank, University of Barcelona, Spain.
Methods Find Exp Clin Pharmacol. 1992 Dec;14(10):781-7.
Thirty young-adult mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) 30 mg/kg/day for 2 days and sacrificed 24 hours later in order to determine striatal catecholamines and to study morphological changes in the nigrostriatal pathway. Immunohistological techniques were also used with polyclonal antibodies for glial fibrillary acidic protein (GFAP) and tyrosine hydroxylase (TH), and monoclonal antibodies for two subunits of neurofilaments. Silver impregnation demonstrated conspicuous neuronal changes affecting cellular processes from substantia nigra in all treated mice. Terminal and axonal degeneration were also observed in striata. These changes were associated with a moderate to marked gliosis. The TH immunoreactivity was normal in cell bodies of substantia nigra but was decreased in striata from MPTP-treated mice. These data indicate that in mice the deterioration of dendritic and axonal neuropil may constitute a significant causal factor of MPTP neurotoxicity.
30只成年小鼠每天按30mg/kg的剂量给予1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP），持续2天，24小时后处死，以测定纹状体儿茶酚胺并研究黑质纹状体通路的形态学变化。还使用免疫组织学技术，采用针对胶质纤维酸性蛋白（GFAP）和酪氨酸羟化酶（TH）的多克隆抗体，以及针对神经丝两个亚基的单克隆抗体。银浸染显示，所有接受治疗的小鼠中，黑质的细胞突起均出现明显的神经元变化。在纹状体中也观察到终末和轴突变性。这些变化与中度至重度的胶质细胞增生有关。黑质细胞体中的TH免疫反应性正常，但MPTP处理小鼠的纹状体中TH免疫反应性降低。这些数据表明，在小鼠中，树突和轴突神经纤维的退化可能是MPTP神经毒性的一个重要因果因素。
