Potegal M, Ferris C F, Hebert M, Meyerhoff J, Skaredoff L
Department of Medical Neurosciences, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
Neuroscience. 1996 Dec;75(3):869-80. doi: 10.1016/0306-4522(96)00236-9.
Allowing a resident hamster a single "priming" attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a second intruder presented within the next 30 min. We present two lines of evidence identifying the corticomedial amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the corticomedial amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce corticomedial amygdala c-fos expression of the same pattern or magnitude. The corticomedial amygdala contribution to the priming effect involves more than a non-specific arousal, since corticomedial amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the corticomedial amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by corticomedial amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the corticomedial amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the corticomedial amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
让一只实验用仓鼠对同种个体进行一次“启动”攻击，会诱发短暂的攻击性觉醒，这表现为对在接下来30分钟内出现的第二个入侵者的攻击潜伏期缩短和攻击概率增加。我们提供了两条证据，表明皮质内侧杏仁核是介导这种效应的重要位点。（1）攻击启动显著增加了皮质内侧杏仁核中表达免疫细胞化学鉴定的Fos蛋白的神经元数量，但在其他部位没有增加。对无生命物体的追逐和撕咬不会诱导相同模式或程度的皮质内侧杏仁核c-fos表达。皮质内侧杏仁核对启动效应的贡献不仅仅涉及非特异性觉醒，因为皮质内侧杏仁核c-fos表达与运动活动（这种觉醒的标准指标）无关。（2）皮质内侧杏仁核的射频损伤会降低攻击性，最显著的降低发生在更靠前的损伤中。其他行为，包括在跑轮中的类似启动的运动练习效应，不受皮质内侧杏仁核损伤的影响。这些发现表明，攻击启动是一种特异性的攻击效应，是由皮质内侧杏仁核所属神经回路中与Fos相关的变化导致的。从理论角度来看，这些实验为分析攻击行为及其持续性背后的机制提出了一种新方法。我们提出了一个定量神经行为模型的概述，该模型将攻击概率与皮质内侧杏仁核内的神经激活联系起来。从方法学角度来看，这些实验扩展了将c-fos表达图谱作为一种在中枢神经系统中定位内源性、行为特异性过程的技术的应用。
