Alcohol, benzodiazepine-GABAA receptor complex and aggression: ethological analysis of individual differences in rodents and primates.

K A Miczek, E M Weerts, J F DeBold
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引用次数: 83

Abstract

Research in animals has only recently been successful in reliably mimicking the long-established link between alcohol and heightened aggressive behavior. The present review highlights the large individual differences in the effects of acute low alcohol doses on aggressive behavior in rodent and primate species, paralleling the human condition. Subpopulations of both species show reliable and repeatable enhancement of aggressive behavior when administered low, acute alcohol doses. Statistical analysis of the temporal patterns of aggressive behavior indicate that alcohol prolongs aggressive bouts or "bursts" and increases the number of aggressive behaviors within each burst. However, the latency to initiate attack and the time between aggressive bursts are relatively unaltered by alcohol. These alcohol-induced increases in aggression can be potentiated by benzodiazepine agonists and prevented by antagonists. In addition, highly aggressive animals can be differentiated from nonaggressive ones at the GABAA-benzodiazepine receptor complex. These data suggest an important link between alcohol, aggression and the GABAA-benzodiazepine receptor complex.

酒精,苯二氮卓- gabaa受体复合物和攻击:啮齿动物和灵长类动物个体差异的行为学分析。
直到最近,对动物的研究才成功地模拟了酒精和攻击性行为加剧之间长期存在的联系。本综述强调了急性低剂量酒精对啮齿动物和灵长类动物攻击行为影响的巨大个体差异,与人类的情况相似。当给予低急性酒精剂量时,这两个物种的亚种群都表现出可靠和可重复的攻击行为增强。对攻击行为时间模式的统计分析表明,酒精延长了攻击发作或“爆发”,并增加了每次爆发中攻击行为的数量。然而,开始攻击的潜伏期和攻击性爆发之间的时间相对来说没有被酒精改变。这些酒精引起的攻击性增加可以通过苯二氮卓类激动剂增强,并通过拮抗剂预防。此外,高攻击性动物可以通过gabaa -苯二氮卓受体复合物与非攻击性动物区分开来。这些数据表明,酒精、攻击性和gabaa -苯二氮卓类受体复合物之间存在重要联系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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