Honey C R, Shen H
Division of Neurosurgery, University of British Columbia, Vancouver, Canada.
Neurosci Lett. 1998 Jun 19;249(2-3):151-4. doi: 10.1016/s0304-3940(98)00431-5.
Rats unilaterally lesioned with 6-hydroxydopamine to deplete striatal dopamine received daily injections of levodopa methyl ester in combination with benserazide. Delayed lesions in the subthalamic nucleus (Group 2) or entopeduncular nucleus and substantia nigra par reticulata (Group 3) were made, unilateral to the dopamine depletion. Apomorphine-induced rotation was significantly reduced in Group 2 versus sham-operated controls (P < 0.006) and in Group 3 versus Group 2 (P < 0.03). Results suggest that enhanced apomorphine-induced rotation in this model is mediated through both the striatopallidal and striatonigral pathway.
用6-羟基多巴胺单侧损伤大鼠以耗尽纹状体多巴胺,这些大鼠每日接受左旋多巴甲酯与苄丝肼联合注射。在多巴胺耗竭的对侧,对丘脑底核(第2组)或脚内核和黑质网状部(第3组)进行延迟损伤。与假手术对照组相比,第2组阿扑吗啡诱导的旋转显著降低(P < 0.006),与第2组相比,第3组阿扑吗啡诱导的旋转显著降低(P < 0.03)。结果表明,该模型中阿扑吗啡诱导的旋转增强是通过纹状体苍白球和纹状体黑质通路介导的。