Anticonvulsant drug mechanisms. Phenytoin, phenobarbital, and ethosuximide and calcium flux in isolated presynaptic endings.
Anticonvulsant drug mechanisms. Phenytoin, phenobarbital, and ethosuximide and calcium flux in isolated presynaptic endings.
复制标题
抗惊厥药物机制。
DOI：
10.1001/archneur.1976.00500090032006
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发表时间：
1976
影响因子：
--
通讯作者：
J. Ferrendelli
中科院分区：
文献类型：
--
作者：
R. S. Sohn;J. Ferrendelli
评估了苯妥英、苯巴比妥、乙舒酰亚胺和盐酸普鲁卡因抑制 Ca2+ 流入从兔新皮质制备的分离突触前末梢（突触体）的能力。苯妥英、苯巴比妥或普鲁卡因可抑制去极化浓度 (69 mM) K+ 产生的钙流入 7% 至 63%，而乙磺酰亚胺则无效。使用低至 0.08 mM 苯妥英和 0.04 mM 苯巴比妥时观察到 Ca2+ 流入减少。相比之下，需要 4 mM 普鲁卡因才能产生效果。这些结果得出这样的结论：产生膜稳定的能力并不是所有抗惊厥药物都具有的特性；然而，这种特性对于有效治疗严重癫痫发作的药物的作用可能至关重要。
Phenytoin, phenobarbital, ethosuximide, and procaine hydrochloride were evaluated for their ability to inhibit Ca2+ flux into isolated presynaptic endings (synaptosomes) prepared from rabbit neocortex. Calcium influx produced by depolarizing concentrations (69 mM) of K+ was inhibited 7% to 63% by phenytoin, phenobarbital, or procaine, whereas ethosuximide was ineffective. Decreased Ca2+ influx was observed with as little as 0.08 mM phenytoin and 0.04 mM phenobarbital. In contrast, 4 mM procaine was needed to produce an effect. These results lead to the conclusion that ability to produce membrane stabilization is not a property of all anticonvulsant drugs; however, this property may be essential for the action of drugs effective in the treatment of major seizures.