Yong V W, Perry T L, Godolphin W J, Jones K A, Clavier R M, Ito M, Foulks J G
Neurotoxicology. 1986 Spring;7(1):19-24.
In an attempt to produce an animal model of Parkinson's disease, we injected rats repeatedly with high doses of methylcyclopentadienyl manganese tricarbonyl (MMT), a compound which has been reported to lower striatal dopamine content in mice. Chronic MMT administration for up to 5 months, even though it produced a substantial elevation in brain manganese content during the period of exposure, did not destroy dopaminergic nigrostriatal neurons. This was assessed by measurements of tyrosine hydroxylase activity and contents of dopamine and its metabolites in the striatum, and by histological examination of the substantia nigra. Our results differ from those of others who administered manganese chloride in drinking water to rats. This discrepancy is unlikely to be a consequence of differences in duration of exposure or route of administration. It could be due to our having used an organic rather than an inorganic manganese compound, or to a species difference in vulnerability to organic manganese between rats and mice.
为了建立帕金森病的动物模型,我们给大鼠反复注射高剂量的甲基环戊二烯三羰基锰(MMT),据报道该化合物可降低小鼠纹状体中的多巴胺含量。连续5个月给予慢性MMT,尽管在暴露期间脑锰含量大幅升高,但并未破坏多巴胺能黑质纹状体神经元。这通过测量纹状体中酪氨酸羟化酶活性、多巴胺及其代谢产物的含量以及对黑质进行组织学检查来评估。我们的结果与其他给大鼠饮用含氯化锰水的研究结果不同。这种差异不太可能是由于暴露持续时间或给药途径的不同造成的。这可能是因为我们使用的是有机而非无机锰化合物,或者是大鼠和小鼠对有机锰的易感性存在种属差异。