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通过电休克或足部电击应激激活内源性阿片系统可抑制大鼠复发性点燃癫痫发作。

Activating endogenous opioid systems by electroconvulsive shock or footshock stress inhibits recurrent kindled seizures in rats.

作者信息

Shavit Y, Caldecott-Hazard S, Liebeskind J C

出版信息

Brain Res. 1984 Jul 9;305(2):203-7. doi: 10.1016/0006-8993(84)90426-8.

Abstract

Electroconvulsive shock (ECS) significantly decreased the behavioral manifestations of seizures elicited by amygdaloid stimulation in kindled rats. This anticonvulsant effect was significantly reduced by the opiate antagonist, naloxone, and by the development of morphine tolerance. A form of footshock stress known to cause opioid-mediated analgesia had a similar anticonvulsant effect, whereas another form causing non-opioid analgesia did not. These results suggest that the anticonvulsant effects of ECS and stress are mediated by the release of endogenous opioids.

摘要

电惊厥休克(ECS)显著降低了点燃大鼠杏仁核刺激诱发癫痫发作的行为表现。阿片类拮抗剂纳洛酮以及吗啡耐受性的形成显著降低了这种抗惊厥作用。一种已知可引起阿片类介导镇痛的足部电击应激形式具有类似的抗惊厥作用,而另一种引起非阿片类镇痛的形式则没有。这些结果表明,ECS和应激的抗惊厥作用是由内源性阿片类物质的释放介导的。

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