单胺能激动剂对酒精诱导小鼠攻击性增加的影响。

G C Wagner, H Fisher, N Pole, T Borve, S K Johnson
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引用次数: 16

摘要

两组研究都是关于酒精引起的攻击性增加。在第一项研究中,研究人员对喂食标准饮食或补充0.5% l -色氨酸的小鼠进行了酒精对目标咬伤和入侵者攻击的影响评估。老鼠在尾部电击后攻击无生命目标的频率高,在电击间隔期间攻击无生命目标的频率中等,在电击前的音调期间攻击无生命目标的频率低。酒精增加了休克后和休克间期的咬伤目标,色氨酸部分阻断了这一作用。常驻小鼠每10分钟攻击入侵者27.2 +/- 5.3次,平均延迟155 +/- 42秒。酒精增加了攻击次数,降低了第一次攻击的延迟时间。色氨酸再次部分阻断了这些作用。最后,在第二组小鼠中,同样的色氨酸饮食被发现增强了氟西汀和芬氟拉明减少攻击的效果,而不破坏运动表现。在第二项研究中,在居住者-入侵者范式中评估了单独使用酒精或与酪胺联合使用酒精的效果。再次观察到,低剂量的酒精增加了入侵者的常驻攻击。虽然联合使用酪胺增强了这种效果,但效果没有达到统计学意义。这些观察结果讨论了酒精引起的进攻性和防御性攻击的增加,以及大脑单胺对这种影响的可能调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of monoaminergic agonists on alcohol-induced increases in mouse aggression.

Two sets of studies were conducted on alcohol-induced increases in aggression. In the first, the effects of alcohol on target biting and resident-intruder attack were assessed in mice fed a standard diet or one supplemented with 0.5% L-tryptophan. Mice attacked an inanimate target at a high rate following tail shock, an intermediate rate during the intershock interval and a low rate during a tone that preceded the shock. Alcohol increased target biting following shock and during the intershock interval, an effect partially blocked by tryptophan. Resident mice attacked intruders 27.2 +/- 5.3 times per 10-minute session with an average latency of 155 +/- 42 seconds. Alcohol increased the number of attacks and lowered the latency to the first attack. Again, tryptophan partially blocked these effects. Finally, in a second set of mice, the same tryptophan diet was found to potentiate the aggression-reducing effects of fluoxetine and fenfluramine without disrupting motor performance. In the second study, the effects of alcohol administered alone or in combination with tyramine were assessed in the resident-intruder paradigm. Again, it was observed that low doses of alcohol increased the resident attack of intruders. Although this effect was heightened by the co-administration of tyramine, the effect failed to reach statistical significance. These observations are discussed in reference to alcohol-induced increases in offensive and defensive aggression and the possible modulation of this effect by brain monoamines.

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