Amagasa M, Mizoi K, Ogawa A, Yoshimoto T
Division Neurosurgery, Tohoku University School of Medicine, Sendai, Japan.
Brain Res. 1989 Dec 11;504(1):87-93. doi: 10.1016/0006-8993(89)91601-6.
A study was made of the protective effects of several drugs (mannitol, phenytoin, vitamin E and dexamethasone) on the electrical activities of guinea pig hippocampal neurons in vitro when they were treated with a bathing medium deprived of both oxygen and glucose. Using guinea pig hippocampal slices, antidromic field potentials in the granular cell layer of the dentate gyrus were recorded stimulating mossy fibers. A model of ischemia in vivo in the slices was achieved by removing both oxygen and glucose from the perfusing medium. In standard medium, after 10 min of both oxygen and glucose deprivation, the field potentials exhibited minimum recovery with an amplitude of 6% of the control after 60 min. The protective effect of the drugs was evaluated by recovery of the field potential amplitude of the 60 min post-deprivation response and histological examination of the brain slice tissue. Drugs were added during 30 min of pre-deprivation and during deprivation. In this experiment we demonstrated that (1) phenytoin and vitamin E clearly showed protective action against neuronal damage caused by both oxygen and glucose deprivation in guinea pig hippocampal slices, (2) combined application of these drugs was more effective, and (3) mannitol showed no protective action in vitro. It was also demonstrated that (4) the dentate antidromic field response can be a useful index of cell death.
本研究观察了几种药物（甘露醇、苯妥英、维生素E和地塞米松）对体外培养的豚鼠海马神经元电活动的保护作用，这些神经元在缺乏氧气和葡萄糖的浴液中受到处理。使用豚鼠海马脑片，通过刺激苔藓纤维记录齿状回颗粒细胞层的逆向场电位。通过从灌注液中去除氧气和葡萄糖，在脑片中建立了体内缺血模型。在标准培养基中，在缺氧和缺糖10分钟后，场电位恢复最小，60分钟后幅度为对照的6%。通过剥夺后60分钟场电位幅度的恢复以及脑片组织的组织学检查来评估药物的保护作用。在剥夺前30分钟和剥夺期间添加药物。在本实验中，我们证明：（1）苯妥英和维生素E对豚鼠海马脑片中由缺氧和缺糖引起的神经元损伤具有明显的保护作用；（2）联合应用这些药物更有效；（3）甘露醇在体外无保护作用。还证明：（4）齿状回逆向场反应可作为细胞死亡的有用指标。
