Aziz T Z, Peggs D, Agarwal E, Sambrook M A, Crossman A R
Department of Cell and Structural Biology, Medical School, Manchester, UK.
Br J Neurosurg. 1992;6(6):575-82. doi: 10.3109/02688699209002375.
Research into the neural mechanisms underlying the symptoms of parkinsonism utilizing the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed primate model have shown that the subthalamic nucleus (STN) occupies a central role. As a logical development of this theory, we have studied the effects of thermocoagulative lesions of the STN in the primate model. Such lesions can cause remarkable symptom reversal in the experimental primate model.
利用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的灵长类动物模型对帕金森综合征症状背后的神经机制进行的研究表明,丘脑底核(STN)起着核心作用。作为该理论的合理拓展,我们研究了在灵长类动物模型中丘脑底核热凝损伤的影响。这种损伤可使实验灵长类动物模型的症状显著逆转。