[阿非尼在小鼠体内独特的精神药理学特征]。

Journal de pharmacologie Pub Date : 1986-01-01
F A Rambert, J Pessonnier, J E de Sereville, A M Pointeau, J Duteil
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引用次数: 0

摘要

阿德拉非尼在小鼠中观察到以下精神药理学作用:增加运动活动(64-256 mg.kg-1),拮抗巴比酮而戊巴比酮的催眠作用(16-128 mg.kg-1),减少强迫游泳试验中不动时间(16-256 mg.kg-1);对电休克有轻微拮抗作用(256 mg.kg-1);直肠温度无改变;没有刻板印象或攀爬行为;未增加聚集小鼠的致死率(分离LD50 = 1022 mg)。kg-1, LD50聚集= 859 mg.kg-1);对抗抑郁药的临时试验缺乏影响:与利血平、氧tremorine或阿吗啡诱导的低温无相互作用,但育亨宾诱导的毒性增强;缺乏外周交感神经效应(无瞳孔、无流涎、无引颈运动肌收缩、无利血平诱导的上睑下垂拮抗作用);缺乏外周抗胆碱能作用(无虫病,无氧tremorine诱导的唾液分泌或流泪的拮抗作用)。与无镇痛药、抗胆碱能药物或抗抑郁药物相比,阿德拉非尼在小鼠身上表现出独特的行为特征,一方面,它具有与抗抑郁类药物作用相关的特定兴奋活性,而这种作用似乎与β -肾上腺素能机制无关,另一方面,它缺乏多巴胺能作用。大多数阿德拉非尼诱导的效应(运动活动增加,强迫游泳试验中静止时间缩短)可能与中枢α 1-肾上腺素能刺激相对应,但外周交感神经效应的意外缺乏仍未得到解释。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[A unique psychopharmacologic profile of adrafinil in mice].

The following psychopharmacological effects of adrafinil have been observed in mice: increase in locomotor activity (64-256 mg.kg-1), antagonism (16-128 mg.kg-1) of the hypnotic effects of barbitone but not of pentobarbitone, reduction of immobility duration in the forced swimming test (16-256 mg.kg-1); slight antagonism (256 mg.kg-1) of electroshock-induced convulsions; no modification of rectal temperature; no stereotyped or climbing behaviour; no increase in lethality in aggregated mice (LD50 isolated = 1022 mg.kg-1, LD50 aggregated = 859 mg.kg-1); lack of effects on the provisional tests for antidepressants: no interaction with reserpine-, oxotremorine-, or apomorphine-induced hypothermia but potentiation of yohimbine-induced toxicity; lack of peripheral sympathetic effects (no mydriasis, no salivation, no contraction of the pilomotor muscles, no antagonism of reserpine-induced ptosis); lack of peripheral anticholinergic effects (no mydriasis, no antagonism of oxotremorine-induced salivation or lacrimation). As compared to no analeptic, anticholinergic or antidepressant drugs, adrafinil shows a unique behavioural profile in mice defined on the one hand by a specific stimulant activity associated with antidepressant-like effects that do no seem related to a beta-adrenergic mechanism and on the other hand by a lack of dopaminergic effects. Most adrafinil-induced effects (increase in locomotor activity, reduction of immobility duration in the forced swimming test) may correspond to a central alpha 1-adrenergic stimulation, but the unexpected lack of peripheral sympathetic effects remains unexplained.

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