Melamed E, Rosenthal J, Globus M, Cohen O, Frucht Y, Uzzan A
Eur J Pharmacol. 1985 Aug 7;114(1):97-100. doi: 10.1016/0014-2999(85)90528-x.
In C57 black mice, MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (30 mg/kg X 2, 20 mg/kg X 15, 30 mg/kg X 15, or 35 mg/kg X 1) depleted DA in both striatum and accumbens but not in frontal cortex, hypothalamus and retina. DA decreases were more pronounced in striatum than in accumbens, were maximal at 2 days, partially reversed later but persisted up to 30 days after treatment. DA depletions in nigra were smaller earlier and maximal later. The study suggests that, in mice, MPTP damages nigrostriatal and mesolimbic projections but spares other DA neurons.
在C57黑鼠中，MPTP（N-甲基-4-苯基-1,2,3,6-四氢吡啶）（30毫克/千克×2次、20毫克/千克×15次、30毫克/千克×15次或35毫克/千克×1次）使纹状体和伏隔核中的多巴胺耗竭，但未使额叶皮质、下丘脑和视网膜中的多巴胺耗竭。纹状体中的多巴胺减少比伏隔核中更明显，在第2天达到最大值，之后部分恢复，但在治疗后30天仍持续存在。黑质中的多巴胺耗竭在早期较小，后期达到最大值。该研究表明，在小鼠中，MPTP损害黑质纹状体和中脑边缘投射，但不影响其他多巴胺能神经元。
