Tsuchiya T, Fukushima H, Kitagawa S
Nihon Yakurigaku Zasshi. 1976 Oct;72(7):861-77.
Effects of clonazepam, nitrazepam and diazepam on penicillin induced primary, spread and reactive epileptoform discharges were investigated in gallamine immobilized cats. Different strengths of seizure foci were induced by penicillin G 1000, 3000 and 6000 U injected into the cortex, amygdala and intralaminal thalamus, and the spread of epileptic discharges in the subcortex or surrounding area and to the contralateral area was followed. Benzodiazepines 5 mg/kg i.v. shortened the duration of primary epileptoform discharges and prolonged the interictal interval in the cortical, amygdaloid and intralaminal thalamic epileptogenesis induced by a high concentration of penicillin G. When a low concentration of penicillin G was injected into the cortex, amygdala and intralaminal thalamus, benzodiazepines abolished the spread of primary epileptoform discharges and the reactive discharges, but did not suppress completely the primary epileptogenic discharges and the contralateral reflective activity. Suppression of the discharges necessitated administration of a high dose. The greatest degree of suppression was seen with clonazepam. It is concluded that the anticonvulsive effect of benzodiazepines may be due to the blackades of neuronal pathways which spread the seizure discharges from the site of origin (focus) to the effector organ, and the elevation of convulsive thresholds.
在加拉明麻醉的猫身上研究了氯硝西泮、硝西泮和地西泮对青霉素诱发的原发性、扩散性和反应性癫痫样放电的影响。通过向皮质、杏仁核和丘脑板内核注射1000、3000和6000单位的青霉素G诱导不同强度的癫痫病灶,并跟踪癫痫放电在皮质下或周围区域以及向对侧区域的扩散。静脉注射5mg/kg的苯二氮䓬类药物可缩短高浓度青霉素G诱发的皮质、杏仁核和丘脑板内核癫痫发生中原发性癫痫样放电的持续时间,并延长发作间期。当向皮质、杏仁核和丘脑板内核注射低浓度的青霉素G时,苯二氮䓬类药物可消除原发性癫痫样放电的扩散和反应性放电,但不能完全抑制原发性致痫放电和对侧反射活动。抑制放电需要给予高剂量药物。氯硝西泮的抑制程度最大。结论是,苯二氮䓬类药物的抗惊厥作用可能是由于阻断了将癫痫放电从起源部位(病灶)传播到效应器官的神经通路,以及提高了惊厥阈值。