Kryzhanovskiĭ G N, Shandra A A, Makul'kin R F, Godlevskiĭ L S, Moiseev I N
Biull Eksp Biol Med. 1985 Oct;100(10):407-10.
Experiments were carried out on random-bred white rats (250-350 g). Kindling was induced by daily intraperitoneal corazol injections in subthreshold (subconvulsive) doses (30 mg/kg). It has been demonstrated that bilateral hippocampal destruction did not change the seizure threshold, while bilateral caudate nucleus destruction lowered it. Hippocampal destruction delayed corazol kindling development and also accelerated the lowering of seizure susceptibility after corazol injections were discontinued, as compared to control animals. Caudate nucleus destruction induced more marked seizure reactions in the first 14 days after corazol injections were started. There were no significant differences in seizure manifestation severity in kindled and control groups. These data point to an essential role of caudate nucleus as an element of antiepileptic system and support the concept that hippocampus plays a role of pathologic determinant which is associated with the formation of an epileptic system underlying corazol kindling.
实验选用随机繁殖的白色大鼠（体重250 - 350克）。通过每日腹腔注射阈下（亚惊厥）剂量（30毫克/千克）的可拉佐来诱发点燃效应。结果表明，双侧海马体损毁并未改变癫痫发作阈值，而双侧尾状核损毁则降低了该阈值。与对照动物相比，海马体损毁延缓了可拉佐点燃效应的发展，并且在停止注射可拉佐后，也加速了癫痫易感性的降低。在开始注射可拉佐后的前14天，尾状核损毁诱发了更为明显的癫痫反应。点燃组和对照组在癫痫发作表现的严重程度上没有显著差异。这些数据表明尾状核作为抗癫痫系统的一个要素起着重要作用，并支持这样一种观点，即海马体起到了病理决定因素的作用，这与可拉佐点燃效应背后癫痫系统的形成有关。
