Frenk H, Liban A, Balamuth R, Urca G
Brain Res. 1982 Dec 16;253(1-2):253-61. doi: 10.1016/0006-8993(82)90692-8.
The intraperitoneal administration of morphine hydrochloride at doses of 300 mg/kg produced analgesia, catalepsy, and electrographic spiking in rats that developed into electrographic seizure patterns after approximately 2.5 h. Whereas naltrexone (12 mg/kg) reversed analgesia and catalepsy, and diminished electrographic spiking, it precipitated electrographic seizure activity similar to that observed following intraperitoneal morphine alone. These seizures were accompanied by behavioral convulsions. No tolerance to these seizures developed with repeated paired administration of morphine and naltrexone or in morphine tolerant rats, but rather potentiation was observed. The epileptogenic effects were found to be potentiated in amygdaloid kindled rats, as well. It was concluded that morphine at these doses activates two different epileptogenic mechanisms, one mediated by opiate receptors, the other not. The possibility of the simultaneous activation of a morphine sensitive anticonvulsant mechanism is discussed.
以300mg/kg的剂量腹腔注射盐酸吗啡可使大鼠产生镇痛、僵住症和电图尖峰,约2.5小时后发展为电图癫痫发作模式。而纳曲酮(12mg/kg)可逆转镇痛和僵住症,并减少电图尖峰,但它会引发与单独腹腔注射吗啡后观察到的类似的电图癫痫活动。这些癫痫发作伴有行为性惊厥。重复联合给予吗啡和纳曲酮或在吗啡耐受的大鼠中,并未产生对这些癫痫发作的耐受性,反而观察到增强作用。在杏仁核点燃的大鼠中,致癫痫作用也被增强。得出的结论是,这些剂量的吗啡激活了两种不同的致癫痫机制,一种由阿片受体介导,另一种则不是。同时还讨论了同时激活吗啡敏感的抗惊厥机制的可能性。