Miczek K A, Weerts E M, DeBold J F
Department of Psychology, Tufts University, Medford, Massachusetts 02155.
J Stud Alcohol Suppl. 1993 Sep;11:170-9. doi: 10.15288/jsas.1993.s11.170.
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.
直到最近,动物研究才成功可靠地模拟出长期以来酒精与攻击性行为增强之间的联系。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性行为影响的巨大个体差异,这与人类情况相似。这两个物种的亚群体在给予低剂量急性酒精时,攻击性行为会出现可靠且可重复的增强。对攻击性行为时间模式的统计分析表明,酒精会延长攻击发作或“爆发”时间,并增加每次爆发中攻击行为的数量。然而,酒精对发起攻击的潜伏期和攻击爆发之间的时间影响相对较小。这些酒精诱导的攻击性增加可被苯二氮䓬激动剂增强,被拮抗剂阻止。此外,在GABAA-苯二氮䓬受体复合物方面,高攻击性动物可与非攻击性动物区分开来。这些数据表明酒精、攻击性和GABAA-苯二氮䓬受体复合物之间存在重要联系。