Matsumura M
Chuo Gunma Neurosurgery Hospital, Takasaki, Japan.
Stereotact Funct Neurosurg. 2001;77(1-4):91-7. doi: 10.1159/000064603.
Early in the 1960s the primate model of Parkinson's disease was first introduced by placing an electrolytic lesion in the midbrain. In the 1980s, a dopaminergic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was accidentally shown to induce parkinsonism in humans, and subsequently was confirmed to reproduce an almost perfect model of parkinsonism in primates. In the late 1980s chemical manipulations of the basal ganglia were shown to induce parkinson symptoms, especially dyskinesia, and more recently, chemical lesioning of the pedunculopontine tegmental nucleus has also been shown to induce parkinsonism. We still do not have a perfect animal model of parkinsonism, however, these models have offered excellent opportunities to study the basic mechanisms in parkinsonism and the function of the basal ganglia.
20世纪60年代初，帕金森病的灵长类动物模型首次通过在中脑放置电解损伤来引入。20世纪80年代，一种多巴胺能神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）意外地被发现可在人类中诱发帕金森综合征，随后被证实能在灵长类动物中重现几乎完美的帕金森综合征模型。20世纪80年代末，对基底神经节的化学操作被证明可诱发帕金森症状，尤其是运动障碍，最近，脚桥被盖核的化学损伤也被证明可诱发帕金森综合征。然而，我们仍然没有一个完美的帕金森综合征动物模型，不过，这些模型为研究帕金森综合征的基本机制和基底神经节的功能提供了绝佳的机会。
