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地西泮对小鼠六种药物诱发的运动性活动亢进的影响(作者译)

[Effects of diazepam on six drug-induced locomotor hyperactivities in mice (author's transl)].

作者信息

Soubrié P, Simon P, Boissier J R

出版信息

Psychopharmacologia. 1975 Dec 31;45(2):197-201. doi: 10.1007/BF00429061.

DOI:10.1007/BF00429061
PMID:129788
Abstract

Experiments were carried out in mice to investigate the influence of diazepam (DZP) on dexamphetamine, parachloro-N-methylamphetamine (pCMA), cocaine, morphine, trihexyphenidyl or (in MAOIs pretreated) reserpine induced motor hyperactivity. The interaction of DZP with these hyperactivities in which probably different biochemical central mechanisms are involved allows to construct a profile of action of DZP and to approach its mechanism of action. The locomotor hyperactivities induced by dexamphetamine, pCMA, morphine, cocaine were not reduced by DZP even by doses which decrease spontaneous locomotor activity; low doses of DZP enhance the hyperactivity induced by these compounds. Those induced by trihexyphenidyle or by reserpine (after MAOI) were reduced by DZP at doses which produce no decrease in spontaneous motor activity. Inasmuch as DZP at low doses potentiates the effects of 4 different substances, the results can hardly be satisfactorily explained neither by an interference of the benzodiazepine on the metabolism of the drugs or by a depression of the anxiogenic action of dexamphetamine. Even though it may be difficult to relate the antagonism of DZP on trihexyphenidyl- or on reserpine- (after MAOI) induced motor hyperactivity to the suggested anticholinergic and dopaminergic actions of DZP, these effects may partly be involved in the increase in locomotor hyperactivity induced by dexamphetamine, morphine, or cocaine. The observed effect of DZP on pCMA induced locomotor hyperactivity does not support a possible antiserotonine action often suggested to explain the effects of benzodiazepines in conflict situations.

摘要

在小鼠身上进行了实验,以研究地西泮(DZP)对右旋苯丙胺、对氯-N-甲基苯丙胺(pCMA)、可卡因、吗啡、苯海索或(在单胺氧化酶抑制剂预处理后)利血平诱导的运动亢进的影响。DZP与这些可能涉及不同生化中枢机制的运动亢进之间的相互作用,有助于构建DZP的作用谱并探究其作用机制。右旋苯丙胺、pCMA、吗啡、可卡因诱导的运动亢进,即使是能降低自发运动活性的剂量,DZP也不能使其降低;低剂量的DZP会增强这些化合物诱导的运动亢进。苯海索或利血平(单胺氧化酶抑制剂处理后)诱导的运动亢进,在不降低自发运动活性的剂量下,DZP可使其降低。由于低剂量的DZP能增强4种不同物质的作用,这些结果很难通过苯二氮䓬对药物代谢的干扰或对右旋苯丙胺致焦虑作用的抑制来令人满意地解释。尽管可能难以将DZP对苯海索或利血平(单胺氧化酶抑制剂处理后)诱导的运动亢进的拮抗作用与DZP所提示的抗胆碱能和多巴胺能作用联系起来,但这些作用可能部分参与了右旋苯丙胺、吗啡或可卡因诱导的运动亢进的增加。观察到的DZP对pCMA诱导的运动亢进的作用,不支持通常认为的苯二氮䓬在冲突情境中的作用可能是抗5-羟色胺作用的观点。

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引用本文的文献

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