Department of Biology, Loyola University Chicago, Chicago, IL 60660, USA.
Physiol Behav. 2010 Apr 19;99(5):562-70. doi: 10.1016/j.physbeh.2010.01.018. Epub 2010 Jan 28.
It has been recently reported that passive exposure to aggression induces aggressive behavior in a rodent model. However, it remains unclear whether this response is correlated with neurochemical changes that correspond either to stress-induced aggression or non-stressed, learned aggression. Stress-induced aggression has been shown to result in increased brain dopamine D(2) receptor and serum corticosterone levels. In contrast, learned aggression is probably associated with reward deficiency syndrome, characterized by low dopamine D(2) receptor levels, without stress effects (i.e., high corticosterone levels). We hypothesized that chronic passive exposure to aggression would produce learned aggression, represented by low levels of dopamine D(2) receptor binding but normal levels of stress hormone. The present study additionally focused on serum testosterone and serotonin 5-HT(1B) receptor density that has been associated with aggression/reward circuits. Hormonal results indicated that there were no differences between the "observer" rats that had been passively exposed to aggression and non-aggression for 10 min/day for 23 consecutive days. However, receptor binding autoradiography identified lower densities of dopamine D(2) receptors in the cortical-accumbal regions (shell of the nucleus accumbens and cingulate and motor cortices) and lower 5-HT(1B) receptor densities in the tegmental regions (ventral tegmental area, substantia nigra pars compacta, and periaqueductal gray) among observers exposed to aggression, compared to controls. Changes in dopamine D(2) receptor densities due to chronic exposure to aggression do not resemble those patterns reported for stress-induced aggressive behavior. Our evidence suggests that the development of aggressive behavior among passive observers occurs through a learned, and not a stress-induced, mechanism.
最近有报道称，被动暴露于攻击行为会在啮齿动物模型中诱发攻击行为。然而，目前尚不清楚这种反应是否与对应于应激诱导攻击或非应激、习得攻击的神经化学变化相关。应激诱导的攻击已被证明会导致大脑多巴胺 D2 受体和血清皮质酮水平增加。相比之下，习得攻击可能与奖励缺乏综合征有关，其特征是多巴胺 D2 受体水平降低，而无应激效应（即皮质酮水平升高）。我们假设慢性被动暴露于攻击会产生习得攻击，表现为多巴胺 D2 受体结合水平降低，但应激激素水平正常。本研究还重点关注了与攻击/奖励回路相关的血清睾酮和 5-羟色胺 5-HT1B 受体密度。激素结果表明，连续 23 天每天被动暴露于攻击或非攻击 10 分钟的“观察者”大鼠之间没有差异。然而，受体结合放射自显影术确定了在皮质-伏隔核区域（伏隔核壳和扣带回和运动皮质）和中脑区域（腹侧被盖区、黑质致密部和导水管周围灰质）中多巴胺 D2 受体密度较低，以及在观察到攻击的观察者中 5-HT1B 受体密度较低，而在对照组中则没有。由于慢性暴露于攻击而导致的多巴胺 D2 受体密度变化与应激诱导攻击行为的报道模式不同。我们的证据表明，被动观察者中攻击行为的发展是通过习得的机制，而不是应激诱导的机制发生的。
