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本研究观察了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－羟基丁酸诱发的实验性失神癫痫发作状态的影响。静脉注射γ－羟基丁酸（２００和４００ｍｇ／ｋｇ）诱发剂量依赖性类失神癫痫发作样行为和脑电变化，其特点是双侧同步的“棘一慢波”，放电频率为１．２８～２．０８Ｈｚ（１．６０±０．１０Ｈｚ）。氯苯氨丁酸使”棘一慢波”放电时间增加，而ＣＧＰ４６３８１则使“棘一慢波”放电时间明显缩短，两者均为剂量依赖性的。静脉单独注射氯苯氨了酸也可引出类失神癫痫发作样行为和脑电变化，“棘一慢波”频率为１．２５～２．３３Ｈｚ（１．７６±０．１２Ｈｚ）。结果提示脑内Ｂ型γ－氨基丁酸能递质活动的增强很可能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 present study investigated the experimental absence of seizures induced by γ-hydroxybutyrate in cynomolgus monkeys treated with GABAergic B receptor agonist chlorbenzuronate and the novel γ-aminobutyric acid B receptor blocker CGP46381 The impact of the state. Intravenous γ-hydroxybutyrate (200 and 400 mg / kg) induced a dose-dependent loss of seizure-like behavior and changes in EEG, which is characterized by bilateral simultaneous “spine-a slow wave” discharge frequency of 1.28 ~ 2.08Hz (1.60 ± 0.10Hz). Chlorbenzidine caused an increase in discharge time for “Spike-Slow Wave” and CGP46381 significantly shortened Spike-Slow Wave discharge time, both of which were dose-dependent. Intravenous injection of chlorpheniramine acid can also lead to loss of absence seizure-like behavior and EEG changes, “spine a slow wave” frequency of 1.25 ~ 2.33Hz (1.76 ± 0.12Hz). The results suggest that the increase of B-type GABAergic neurotransmitter activity in brain may be the main reason of denervation seizures. At the same time, γ-aminobutyric acid B receptor blockers hope to become a new anti-epileptic drugs.