创伤后应激障碍的动物模型及其神经生物学机制

The Animal Models and Neurobiological Mechanisms of Posttraumatic Stress Disorder

创伤后应激障碍是指个体由于经历对生命具有威胁的事件或严重的创伤，导致症状长期持续的精神障碍。研究创伤后应激障碍的主要动物模型为条件性恐惧和应激敏感化模型。研究表明，创伤后应激障碍中长时程留存的恐惧性记忆、高唤醒等症状与大脑杏仁核、内侧前额叶皮层和海马三个脑区及下丘脑-垂体-肾上线轴负反馈功能增强密切相关。其中杏仁核活动增强是条件性恐惧记忆获得、保持和表达的关键神经基础。内侧前额叶皮层对杏仁核的去抑制及海马向杏仁核传递的威胁性环境信息，促进创伤后应激障碍症状的出现。在经历创伤应激后糖皮质激素受体的上调及多巴胺活动的增强是创伤后应激障碍产生的主要神经基础。对创伤后应激障碍的药物治疗研究证明多巴胺D2受体在改善患者症状中的作用比较重要，但仍需作更深入的探索。

Posttraumatic stress disorder（PTSD）is a kind of mental disorder that usually occurs in a delayed manner and lasts long after life-threatened traumas. Studies on animal models of fear conditioning and sensitization show that the symptoms of this disorder， such as fear memory and hyperarousal closely related to the aberrant activities of amygdale， medial prefrontal cortex， hippocampus and hypothalamic-pituitary-adrenal axis. Increased activity of amygdale is critical for acquisition， consolidation and expression of conditioned fear. In addition， decreased inhibition of medial prefrontal cortex on amygdale and the input of threatened information from hippocampus to amygdala facilitate the development of this disorder. The upregulation of glucocorticoid receptors and increased dopaminergic activities after traumas are main neurochemical mechanisms of PTSD. Studies on drug treatment of this disorder show that dopamine D2 receptors are important， but the specific neurobiological underpinnings of PTSD awaits for more explorations.