Kalichman M W
Epilepsia. 1982 Apr;23(2):163-71. doi: 10.1111/j.1528-1157.1982.tb05064.x.
The convulsant potencies of several drugs that antagonize GABAergic neurotransmission were assessed in amygdala-kindled and control rats. The potencies of picrotoxin, pentylenetetrazol, and a convulsant barbiturate were increased by amygdala kindling. No significant potentiation, however, was observed with isoniazid, 3-mercaptopropionic acid, bicuculline, or the glycine antagonist strychnine. Destruction, by electrolytic lesion, of the amygdala focus did not reverse the kindling-induced potentiation of picrotoxin convulsions. The potentiation of picrotoxin convulsions was correlated with the pattern of kindling development but not with the number of stimulations or seizures. The present results are consistent with the hypotheses that (1) kindling potentiates only some convulsant agents, (2) kindling-induced convulsant potentiation takes place outside of the kindled focus, and (3) kindling is not produced by a failure of the GABA system.
在杏仁核点燃大鼠和对照大鼠中评估了几种拮抗γ-氨基丁酸能神经传递的药物的惊厥效力。杏仁核点燃使印防己毒素、戊四氮和一种惊厥性巴比妥酸盐的效力增强。然而，异烟肼、3-巯基丙酸、荷包牡丹碱或甘氨酸拮抗剂士的宁未观察到明显的增强作用。通过电解损伤破坏杏仁核病灶并不能逆转点燃诱导的印防己毒素惊厥增强作用。印防己毒素惊厥的增强与点燃发展模式相关，但与刺激次数或癫痫发作次数无关。目前的结果与以下假设一致：(1) 点燃仅增强某些惊厥剂的作用；(2) 点燃诱导的惊厥增强发生在点燃病灶之外；(3) 点燃不是由γ-氨基丁酸系统功能障碍引起的。
