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MK-801可预防小鼠反复电惊厥治疗引起的对阿扑吗啡行为反应增强。

MK-801 prevents the enhanced behavioural response to apomorphine elicited by repeated electroconvulsive treatment in mice.

作者信息

Nomikos G G, Mathé A A, Mathé J M, Svensson T H

机构信息

Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.

出版信息

Psychopharmacology (Berl). 1992;108(3):367-70. doi: 10.1007/BF02245125.

Abstract

Repeated administration of electroconvulsive stimuli (ECS) to mice once daily for a period of 7 days results in an enhanced locomotor response induced by apomorphine (1.0 mg/kg, IP). Pretreatment (30 min) with the N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (0.01-1.0 mg/kg IP), suppressed ECS-induced seizure activity in a dose-dependent manner. MK-801 (0.01 and 0.033 mg/kg, IP) given 30 min before each ECS dose-dependently decreased apomorphine-mediated responses. Administration of MK-801 (0.033 mg/kg IP) 30 min after each convulsion had the same effect. These results indicate that MK-801 can abolish the ECS-induced enhancement of dopamine-mediated behaviour possibly by interfering with postictal processes. Thus, NMDA receptors seem to be involved in the behavioural changes and presumably also in the neural adaptations produced by repeated ECS.

摘要

每天对小鼠重复给予电惊厥刺激(ECS),持续7天,会导致阿扑吗啡(1.0毫克/千克,腹腔注射)诱导的运动反应增强。用N-甲基-D-天冬氨酸(NMDA)受体拮抗剂MK-801(0.01 - 1.0毫克/千克,腹腔注射)进行预处理(30分钟),可剂量依赖性地抑制ECS诱导的癫痫发作活动。在每次ECS给药前30分钟给予MK-801(0.01和0.033毫克/千克,腹腔注射),可剂量依赖性地降低阿扑吗啡介导的反应。在每次惊厥后30分钟给予MK-801(0.033毫克/千克,腹腔注射)也有相同效果。这些结果表明,MK-801可能通过干扰发作后过程来消除ECS诱导的多巴胺介导行为的增强。因此,NMDA受体似乎参与了行为变化,并且可能也参与了重复ECS产生的神经适应性变化。

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