心理科学进展
心理科學進展
심이과학진전
Advances In Psychological Science
2008年
3期
371~377
,共null页
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
創傷後應激障礙 恐懼條件化 敏感化 多巴胺 下丘腦-垂體-腎上腺軸
창상후응격장애 공구조건화 민감화 다파알 하구뇌-수체-신상선축
Posttraumatic Stress Disorder, fear conditioning, sensitization, dopamine, HPA axis.
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.肾上腺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。
創傷後應激障礙是指箇體由于經歷對生命具有威脅的事件或嚴重的創傷,導緻癥狀長期持續的精神障礙。研究創傷後應激障礙的主要動物模型為條件性恐懼和應激敏感化模型。研究錶明,創傷後應激障礙中長時程留存的恐懼性記憶、高喚醒等癥狀與大腦杏仁覈、內側前額葉皮層和海馬三箇腦區及下丘腦.垂體.腎上腺軸負反饋功能增彊密切相關。其中杏仁覈活動增彊是條件性恐懼記憶穫得、保持和錶達的關鍵神經基礎。內側前額葉皮層對杏仁覈的去抑製及海馬嚮杏仁覈傳遞的威脅性環境信息,促進創傷後應激障礙癥狀的齣現。在經歷創傷應激後糖皮質激素受體的上調及多巴胺活動的增彊是創傷後應激障礙產生的主要神經基礎。對創傷後應激障礙的藥物治療研究證明多巴胺D2受體在改善患者癥狀中的作用比較重要,但仍需作更深入的探索。
창상후응격장애시지개체유우경력대생명구유위협적사건혹엄중적창상,도치증상장기지속적정신장애。연구창상후응격장애적주요동물모형위조건성공구화응격민감화모형。연구표명,창상후응격장애중장시정류존적공구성기억、고환성등증상여대뇌행인핵、내측전액협피층화해마삼개뇌구급하구뇌.수체.신상선축부반궤공능증강밀절상관。기중행인핵활동증강시조건성공구기억획득、보지화표체적관건신경기출。내측전액협피층대행인핵적거억제급해마향행인핵전체적위협성배경신식,촉진창상후응격장애증상적출현。재경력창상응격후당피질격소수체적상조급다파알활동적증강시창상후응격장애산생적주요신경기출。대창상후응격장애적약물치료연구증명다파알D2수체재개선환자증상중적작용비교중요,단잉수작경심입적탐색。
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.