Stone W E, Javid M J
Arch Int Pharmacodyn Ther. 1980 Jan;243(1):56-65.
In its pattern of sensitivity to anticonvulsants, kainic acid (KA) showed little resemblance to pentylenetetrazol (PTZ), 3-mercaptopropionic acid (3-MP), bicuculline, picrotoxin or bemegride. That KA may have an action on the gamma-aminobutyrate system is suggested by the following: it is strongly antagonized by aminooxyacetic acid; ethosuximide is ineffective against KA as it is against 3-MP; and a subconvulsive dose of KA potentiated 3-MP but not PTZ. However, KA is to some extent comparable to PTZ in that it is antagonized by trimethadione, phenobarbital and chlordiazepoxide more effectively than is 3-MP. The convulsive action of KA is potentiated by the glutamate antagonists l-glutamate diethyl ester (GDEE) and l-nuciferine. GDEE also slightly potentiated bicuculline, but not other convulsants tested; it slightly antagonized PTZ. Nuciferine potentiated all except PTZ and bemegride. The failure of these agents to antagonize KA-induced seizures is consistent with the view that KA and glutamate act at separate excitatory receptor sites. The potentiation might possibly be due to a blocking of glutamergic activation of neurons that are inhibitory.
在对抗惊厥药的敏感性模式方面， kainic 酸（KA）与戊四氮（PTZ）、3-巯基丙酸（3-MP）、荷包牡丹碱、印防己毒素或贝美格几乎没有相似之处。以下情况表明 KA 可能对γ-氨基丁酸系统有作用：它被氨氧乙酸强烈拮抗；乙琥胺对 KA 无效，就像对 3-MP 无效一样；亚惊厥剂量的 KA 增强了 3-MP 的作用，但没有增强 PTZ 的作用。然而，KA 在某种程度上与 PTZ 具有可比性，因为它比 3-MP 更有效地被三甲双酮、苯巴比妥和氯氮卓拮抗。KA 的惊厥作用被谷氨酸拮抗剂 l-谷氨酸二乙酯（GDEE）和 l-荷叶碱增强。GDEE 也略微增强了荷包牡丹碱的作用，但没有增强其他测试的惊厥剂的作用；它略微拮抗了 PTZ。荷叶碱增强了除 PTZ 和贝美格之外的所有药物的作用。这些药物未能拮抗 KA 诱导的癫痫发作，这与 KA 和谷氨酸作用于不同的兴奋性受体位点的观点一致。这种增强作用可能是由于阻断了抑制性神经元的谷氨酸能激活。
