Matsumura M, Kojima J
Chuo Gunma Neurosurgery Hospital, Nakaomachi, Takasaki, Japan.
Stereotact Funct Neurosurg. 2001;77(1-4):108-15. doi: 10.1159/000064614.
To clarify the role of the pedunculopontine tegmental nucleus (PPN) in motor behavior, we have conducted a series of experiments in primates. In the first part, PPN was damaged locally with kainic acid, which resulted in mild hemiparkinsonism in the contralateral limbs. In the second part, muscimol (a GABA agonist) was locally injected into the PPN area in monkeys who had been trained to perform a lever-pull movement with an arm, resulting in a slowness of movement and a delay of the movement onset. In the third part, a dopaminergic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was systemically injected in monkeys with prior PPN lesioning. These monkeys developed no, or if any, very mild parkinsonism. PPN lesioning was supposed to have protected the nigral neurons from the MPTP- toxicity. The PPN facilitates the motor system through its nigral projection. The decreased activity of the PPN may underlie the pathophysiology of parkinsonism.
为阐明脚桥被盖核（PPN）在运动行为中的作用，我们在灵长类动物中进行了一系列实验。在第一部分中，用 kainic 酸局部损伤 PPN，这导致对侧肢体出现轻度偏侧帕金森症。在第二部分中，将蝇蕈醇（一种 GABA 激动剂）局部注射到经过训练用手臂进行杠杆拉动运动的猴子的 PPN 区域，导致运动迟缓以及运动起始延迟。在第三部分中，对先前已损伤 PPN 的猴子全身注射多巴胺能神经毒素 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）。这些猴子未出现帕金森症，或者即便出现，也非常轻微。PPN 损伤被认为保护了黑质神经元免受 MPTP 的毒性作用。PPN 通过其向黑质的投射促进运动系统。PPN 活性降低可能是帕金森症病理生理学的基础。
