Pathological aggression, frequently observed in psychiatric patients and criminal subjects, poses a major burden on the health care and criminal justice system, necessitating better aetiological models to inform targets for prevention and intervention. Emerging evidence suggests that adverse experiences during development can cause long-lasting brain alterations associated with maladaptive behaviors, such as aggression. The present review discusses, mainly based on studies in rodents, whether disruption of the mesocorticolimbic dopamine system through chronic stress-exposure during adolescence predisposes to adult aggression. Our findings suggest that chronic stress in adolescence induces prefrontal cortex (PFC) hyperdopaminergia and ultimately leads to blunted prefrontal dopamine transmission in adulthood. This, in turn, disrupts the ability of the PFC to guide adaptive, long-term focused action selection by regulating mesolimbic dopamine signaling. We propose that, especially during the dynamic and transitional period of adolescence, exposure to chronic stress could lead to excessive adaptive change, which may result in an increased vulnerability to maladaptive aggression in adulthood. We discuss how these findings in rodents may translate to humans.

在精神病患者和犯罪主体中经常观察到的病理侵略给医疗保健和刑事司法系统带来了沉重负担，因此需要更好的病因学模型来为预防和干预目标提供信息。越来越多的证据表明，发育过程中的不良经历会导致与不良适应行为（例如攻击性）相关的长期大脑改变。本综述主要基于对啮齿动物的研究，讨论在青春期通过长期暴露于压力而破坏中皮层-寡聚多巴胺系统是否会导致成年侵略。我们的研究结果表明，青春期的慢性应激会诱发前额叶皮层（PFC）多巴胺痛，并最终导致成年期前额叶多巴胺传播减弱。反过来，通过调节中脑边缘多巴胺信号传导，破坏了PFC指导适应性长期集中行动选择的能力。我们建议，尤其是在青春期的动态和过渡时期，暴露于慢性压力下可能导致过度的适应性改变，这可能导致成年人对适应不良的侵略行为的脆弱性增加。我们讨论了在啮齿动物中的这些发现如何可能转化为人类。