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本工作以点燃惊厥大鼠为模型，观察给予氯硝西泮１ｗｋ及４ｗｋ后，其对点燃惊厥大鼠的抗惊作用及抗惊耐受性，并观察了耐受大鼠撤药１ｗｋ后行为改变。同时通过对大鼠脑组织ＧＡＢＡＡ－受体的检测，对其抗惊作用耐受性及依赖性机制进行了研究。结果显示：氯硝西泮对点燃惊厥大鼠有明显的抗惊作用，但长期应用可产生抗惊作用的耐受性，表现为惊厥等级的升高。撤药１ｗｋ后，惊厥等级明显升高，惊厥潜伏期明显缩短。模型大鼠的溶剂对照组较正常Ｗｉｓｔａｒ大鼠的ＧＡＢＡＡ－受体的Ｂｍａｘ值明显降低，而给予氯硝西泮可明显增加Ｂｍａｘ。但长期给予则Ｂｍａｘ降低，撤药１ｗｋ后Ｂｍａｘ又明显增加。提示：氯硝西泮抗点燃惊厥大鼠耐受性与ＧＡＢＡＡ－受体下调有关，而依赖性则与ＧＡＢＡＡ一受体上调有关。
In this work, the model of lit convulsive rats was used to observe the anti-shock effect and anti-shock tolerance of clonazepam administered 1 and 4 weeks after the administration of clonazepam, change. At the same time, the mechanism of anti-shock tolerance and its dependence was studied by detecting GABAA-receptor in rat brain. The results showed that clonazepam had obvious anticonvulsant effects on convulsant-induced convulsions in rats, but its long-term use could produce tolerance to anticonvulsant and showed an increase in seizure grade. 1wk withdrawal, convulsions significantly increased grade, convulsions significantly shortened incubation period. The Bmax of GABAA-receptor in model rats was significantly lower than that of normal Wistar rats, while the treatment with clonazepam significantly increased Bmax. However, Bmax decreased after long-term administration, and Bmax increased significantly after 1wk withdrawal. Tip: clonazepam anticonvulsant convulsive rats tolerance and GABAA-receptor down, while the dependence is associated with a GABAA receptor upregulation.