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[地西泮耐受性的γ-氨基丁酸能机制的病因学研究]

[Etiologic study of the GABAergic mechanisms of diazepam tolerance].

作者信息

Poshivalov V P

出版信息

Farmakol Toksikol. 1981 Sep-Oct;44(5):546-50.

PMID:7308433
Abstract

Etiologic analysis used in experiments on isolated mice has shown that each biologically important category of intraspecies behavior (aggression, communicability, etc) is characterized by its own time course of diazepam tolerance. Participation of the GABAergic mechanisms in acute and chronic effects of diazepam was demonstrated to vary. Acute effect of diazepam was dominated by the sedative component whose action was reversed by picrotoxin and bicuculline that activated motor rather than zoosocial activities. In the course of diazepam tolerance induction, picrotoxin and bicuculline counteracted antiaggressive action of diazepam and diazepam-induced activation of intraspecies communicability. However, they did not fully inhibit the communicability.

摘要

对分离的小鼠进行的实验中所采用的病因分析表明,种内行为的每一个具有生物学重要性的类别(攻击性、社交性等)都有其自身的地西泮耐受性时间进程。已证明GABA能机制在急性和慢性地西泮效应中的参与情况有所不同。地西泮的急性效应以镇静成分占主导,其作用可被苦味毒和荷包牡丹碱逆转,这两种物质激活的是运动而非动物社交活动。在地西泮耐受性诱导过程中,苦味毒和荷包牡丹碱抵消了地西泮的抗攻击作用以及地西泮诱导的种内社交性激活。然而,它们并未完全抑制社交性。

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