Kryzhanovskiĭ G N, Shandra A A, Godlevskiĭ L S, Mazarati A M
Biull Eksp Biol Med. 1990 Jun;109(6):531-4.
In the experiments on rats it was shown that the picrotoxin kindling, which consists of the progressive increasing of convulsive reactions during daily systemic administration of picrotoxin in subconvulsive dosages results also in the development of the pathologically enhanced defensive reactions. The destruction of hippocampal structures by kainic acid prevented the seizure syndrome, while their activation due to blood injection in hippocampus promoted its development; under these conditions the kindling of pathologically enhanced defensive reactions was not significantly changed. Bilateral amygdalar destruction significantly attenuated the development of pathologically increased defensive behavior; under these conditions the seizure syndrome was not significantly changed. The data are discussed on the theory of generator, and systemic mechanisms of neuropathologic syndromes and show that picrotoxin kindling results in the formation of two different pathologic systems which cause the development of two mentioned syndromes: seizure syndrome and syndrome of pathologically enhanced defensive behavior.
在对大鼠的实验中发现,印防己毒素点燃效应,即每日以亚惊厥剂量全身给予印防己毒素期间惊厥反应逐渐增强,也会导致病理性增强的防御反应的发展。海人酸对海马结构的破坏可预防癫痫发作综合征,而向海马内注射血液导致海马结构激活则会促进其发展;在这些条件下,病理性增强的防御反应的点燃效应没有明显变化。双侧杏仁核破坏显著减弱了病理性增强的防御行为的发展;在这些条件下,癫痫发作综合征没有明显变化。根据发生器理论以及神经病理综合征的系统机制对这些数据进行了讨论,结果表明印防己毒素点燃效应导致形成两个不同的病理系统,它们分别引发上述两种综合征:癫痫发作综合征和病理性增强的防御行为综合征。