摘要
目的：观察脑益嗪抗运动病时脑细胞钙离子（Ｃａ２＋）的变化并探讨其作用机理。方法：采用Ｃａ２＋超微结构定位方法，对ＳＤ大鼠预先给予脑益嗪后，采用正负交变加速度旋转刺激制备运动病模型。观察运动病大鼠和脑益嗪给药组大鼠大脑皮质、小脑皮质和脑干前庭区脑细胞Ｃａ２＋超微结构定位变化。结果：运动病大鼠大脑皮质、小脑皮质和脑干前庭区脑细胞质基质、线粒体和内质网中Ｃａ２＋反应产物增多。预先给予脑益嗪后，大脑皮质、小脑皮质和脑干前庭区脑细胞质Ｃａ２＋反应产物明显下降（Ｐ＜０．０１）。
Aim: Examination of the changes of ultrastructural localization of calcium ions in the rat brain during anti-motion sickness use of cinnarizine so as to explore the action mechanism of cinnarizine in the central nervous system. Methods: Ultrastructural Ca^(2+) localization method was used. The SD rats were given cinnarizine(20mg/kg ip) 2.5h prior, then the animals were made motion sickness by means of alternate +/- accelerating rotational stimulation. Changes of ultrastructural localization of Ca^(2+) in the brain cells of the animals were examined; while those animals without receiving cinnarizine were used as control. Results: The reaction products of Ca^(2+) in cytoplamic matrix, mitochondria and endoplasmic reticulum of cerebral cortex, cerebellar cortex and vestibular area of brain stem in the motion sickness group of animals were increased, whereas those in the group having rcceived cinnarizine were markedly decreased. Conclusion: The inhibition of Ca^(2+) introflow in nerve cells of the brain could be one of the central mechanism of cinnarizine in preventing motion sickness.
基金
海军科研基金
关键词
脑益嗪
运动病
钙
前庭刺激
定位
超微结构
Cinnarizine Motion sickness Calcium ion Vestibular stimulation
