Little H J
Pharmacology Department, Medical School, Bristol.
Neuropeptides. 1991 Jul;19 Suppl:11-4. doi: 10.1016/0143-4179(91)90077-v.
Benzodiazepine withdrawal, spontaneous or precipitated by the receptor antagonist, flumazenil, produces anxiety that can be measured in animal models. Benzodiazepine inverse agonists also cause anxiety. Their convulsive effects increase after chronic agonist treatment, but they become anxiolytic. Decreases in GABAA receptor sensitivity occur after chronic benzodiazepine treatment. Flumazenil, given 24h prior to the measurements, prevented both the sensitivity changes and benzodiazepine tolerance in vivo. The anxiety and decreases in seizure threshold during withdrawal were also prevented. It has been suggested that flumazenil causes a prolonged 'resetting' of the benzodiazepine receptor complex. Acute flumazenil decreased anxiety-related behaviour during ethanol withdrawal. Concurrent chronic treatment with verapamil completely prevented anxiety following chronic benzodiazepine treatment.
苯二氮䓬戒断,无论是自发的还是由受体拮抗剂氟马西尼诱发的,都会产生焦虑,这种焦虑在动物模型中是可以测量的。苯二氮䓬反向激动剂也会引起焦虑。在长期使用激动剂治疗后,它们的惊厥作用会增强,但会变成抗焦虑的。长期使用苯二氮䓬治疗后,GABAA受体敏感性会降低。在测量前24小时给予氟马西尼,可防止体内敏感性变化和苯二氮䓬耐受性。戒断期间的焦虑和癫痫阈值降低也得到了预防。有人认为,氟马西尼会导致苯二氮䓬受体复合物的长期“重置”。急性给予氟马西尼可减少乙醇戒断期间与焦虑相关的行为。维拉帕米与慢性治疗同时使用可完全预防长期使用苯二氮䓬治疗后的焦虑。