Corcoran M E, Urstad H, McCaughran J A, Wada J A
Can J Neurol Sci. 1975 Nov;2(4):501-8. doi: 10.1017/s0317167100020643.
To test the hypothesis that the cortex participates in amygdaloid kindling in rats, bilateral aspiration lesions were made in various cortical areas in rats prior to kindling. Lesions in orbital cortex (on the dorsal lip of the rhinal sulcus) or prefrontal cortex (area 10) significantly retarded the rate of amygdaloid kindling; lesions in motor cortex, anterior cingulate cortex, or visual cortex were without effect. Detailed analysis indicated that the orbital lesioned and frontal-lesioned rats kindled relatively normally up to the second-last stage of amygdaloid kindling, in which stage they perseverated significantly longer than the controls and the other lesioned rats. These results suggest that areas of the frontal lobe participate in the elaboration and generalization of amygdaloid seizures in rats. Although retarded in rate, kindling nonetheless occurred in the lesioned rats, indicating that these cortical areas are not essential for the development of amygdaloid seizures.
为了验证大脑皮层参与大鼠杏仁核点燃的假说，在点燃前对大鼠的不同皮层区域进行双侧抽吸损伤。眶皮质（在鼻沟背侧缘）或前额叶皮质（10区）的损伤显著延缓了杏仁核点燃的速度；运动皮质、前扣带回皮质或视觉皮质的损伤则没有效果。详细分析表明，眶损伤和额叶损伤的大鼠在杏仁核点燃的倒数第二阶段之前相对正常地点燃，在这个阶段它们持续的时间比对照组和其他损伤大鼠长得多。这些结果表明，额叶区域参与了大鼠杏仁核癫痫发作的细化和泛化。尽管点燃速度减慢，但损伤大鼠仍发生了点燃，这表明这些皮层区域对于杏仁核癫痫发作的发展并非必不可少。
