关键词: 创伤后应激障碍, 恐惧条件化, 敏感化, 多巴胺, 下丘脑-垂体-肾上腺轴

Abstract: Abstract: 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 amygdala, medial prefrontal cortex, hippocampus and hypothalamic–pituitary–adrenal axis. Increased activity of amygdala is critical for acquisition, consolidation and expression of conditioned fear. In addition, decreased inhibition of medial prefrontal cortex on amygdala 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

Key words: Posttraumatic Stress Disorder, fear conditioning, sensitization, dopamine, HPA axis