Kulkarni S K, Jog M V
Psychopharmacology (Berl). 1983;81(4):332-4. doi: 10.1007/BF00427572.
A subeffective dose (2 mg/kg) of diazepam produced only 50% protection against picrotoxin-induced (PTX) convulsions in rats. Simultaneous administration of GABA and other GABA-ergic substances such as piracetam and sidium valproate, which did not have any effect by themselves, potentiated diazepam action. The onset of convulsions and mortality due to PTX were significantly delayed. The other conventional anticonvulsants phenobarbitone, phenytoin and ethosuximide also enhanced the protective effect of diazepam. Inosine, a putative benzodiazepine ligand, also enhanced diazepam action. These observations are explained on the basis of data from in vitro studies indicating that GABA-ergic agents and barbiturates enhance both the number of benzodiazepine binding sites and benzodiazepine binding. The protective effect of clonidine, however, may be mediated by a different mechanism unrelated to the GABA-ergic system.
地西泮的亚有效剂量（2毫克/千克）仅对大鼠匹鲁卡品诱导的惊厥提供50%的保护作用。同时给予γ-氨基丁酸（GABA）以及其他本身无任何作用的GABA能物质，如吡拉西坦和丙戊酸钠，可增强地西泮的作用。匹鲁卡品诱导的惊厥发作和死亡率显著延迟。其他传统抗惊厥药苯巴比妥、苯妥英和乙琥胺也增强了地西泮的保护作用。肌苷，一种假定的苯二氮䓬配体，也增强了地西泮的作用。这些观察结果基于体外研究数据得到解释，表明GABA能药物和巴比妥类药物可增加苯二氮䓬结合位点的数量并增强苯二氮䓬结合。然而，可乐定的保护作用可能由与GABA能系统无关的不同机制介导。
