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观察了γ－氨基丁酸能Ｂ受体激动剂氯苯氨丁酸和新型γ－氨基丁酸能Ｂ受体阻断剂ＣＧＰ４６３８１对猕猴由γ－烃基丁酸诱发的失神性癫痫发作状态的影响。给猴静脉注射γ－羟基丁酸（２００和４００ｍｇ／ｋｇ）诱发剂量依赖性类失神性癫痫发作样行为和脑电变化，其特点是双侧同步的＂棘－慢波＂，放电频率为１．２８Ｈｚ－２．０８Ｈｚ（１．６０±０．１０Ｈｚ）。氯苯氨丁酸使＂棘－慢波＂放电时间增加，而ＣＧＰ４６３８１则使癫痫的发作率明显降低，两者均为剂量依赖性的。静脉单独注射氯苯氨丁酸也可引出类似失神性癫痫发作的行为和脑电变化，＂棘－慢波＂频率为１．２５Ｈｚ－２．３３Ｈｚ（１．７６±０．１２Ｈｚ）。结果表明脑内Ｂ型γ－氨基丁酸能递质活动的增强是失神性癫痫发作的主要原因。同时，γ－氨基丁酸能Ｂ受体阻断剂有希望成为新型抗癫痫药物。
The effects of GABAergic B receptor agonist chlorbenzuronide and a novel γ-aminobutyric acid B receptor blocker CGP46381 on the deaf condition induced by GABA in macaques were observed . Intravenous γ-hydroxybutyrate (200 and 400 mg / kg) induced a dose-dependent de-seizure-like seizure-like behavior and electroencephalogram changes in monkey that were characterized by bilateral “spike-slow waves” with a firing frequency of 1 .28Hz-2.08Hz (1.60 ± 0.10Hz). Chlorbenzuron increased the spike-slow wave discharge time, whereas CGP46381 significantly reduced the incidence of epilepsy, both of which were dose-dependent. Intravenous injection of clofibrate also led to behavioral and EEG changes similar to denervated seizures, with “spike-slow wave” frequencies ranging from 1.25 Hz to 2.33 Hz (1.76 ± 0.12 Hz). The results show that brain B-type GABA neurotransmitter activity enhancement is the main reason for deafness seizures. At the same time, γ-aminobutyric acid B receptor blockers hope to become a new anti-epileptic drugs.