McIntyre D C, Edson N
Department of Psychology, Carleton University, Ottawa, Ontario, Canada.
Exp Neurol. 1989 Apr;104(1):10-4. doi: 10.1016/0014-4886(89)90002-2.
In two experiments, involvement of norepinephrine in the development of status epilepticus was determined. Rats, pretreated with intraventricular 6-hydroxydopamine to deplete brain norepinephrine or with the saline vehicle alone, were implanted with electrodes in both amygdalae. In the first experiment, one amygdala was kindled to stage 5 levels and then 2 weeks later was stimulated continuously for 60 min in an effort to produce status epilepticus (SE), while in the second experiment such SE stimulation was applied to one amygdala without prior kindling. Although depletion of norepinephrine significantly facilitated amygdala kindling in experiment 1, it had no clear effect on the probability of developing SE (generalized, partial, or nonconvulsive) or on the distribution of gross brain pathology following spontaneous recovery from partial and nonconvulsive SE in either experiment. The significance of these results compared to other SE models was discussed.
在两项实验中，确定了去甲肾上腺素在癫痫持续状态发展中的作用。给大鼠脑室内注射6-羟基多巴胺以耗尽脑内去甲肾上腺素，或仅注射生理盐水作为对照，然后在双侧杏仁核植入电极。在第一个实验中，将一侧杏仁核点燃至5级水平，2周后持续刺激60分钟以诱发癫痫持续状态（SE），而在第二个实验中，对一侧杏仁核直接进行SE刺激，不预先点燃。尽管在实验1中去甲肾上腺素的耗竭显著促进了杏仁核点燃，但在两个实验中，它对SE（全身性、部分性或非惊厥性）发生的概率或部分性和非惊厥性SE自发恢复后脑大体病理学分布均无明显影响。讨论了这些结果与其他SE模型相比的意义。
