神经生物学的恐惧,焦虑和灭绝:对心理治疗Neurobiology of Fear, Anxiety and Extinction: Implications for Psychotherapy |
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课程网址: | http://videolectures.net/mitworld_davis_nfae/ |
主讲教师: | Michael Davis |
开课单位: | 埃默里大学 |
开课时间: | 2010-10-20 |
课程语种: | 英语 |
中文简介: | 很少有科学家以与迈克尔戴维斯相同的顽强和精确的方式描绘了恐惧和焦虑的严峻领域。近四十年前,研究人员了解到,包括人类在内的动物在恐惧时会更加惊讶。例如,在一个黑暗,令人毛骨悚然的小巷中突然发出的噪音引起了比在光线充足的房间里更大的反应。这让戴维斯和他的同事们想知道惊恐反射背后的神经机制是什么,以及恐惧如何在反应中发挥作用。在他的演讲中,戴维斯描述了他和其他人多年来进行的细致实验。从恐惧强化的惊吓测试开始 - 研究人员训练动物将光线或声音等刺激与震动配对 - 研究人员开始追踪调节神经系统反应的途径。使用可跟踪大脑电活动的化学示踪剂,戴维斯在杏仁核的中央核中发现了一组对恐惧条件反射至关重要的细胞。 “这是在实验室里度过的美好时光,”他说。当他用药物或病变击倒这部分杏仁核时,它选择性地减少了恐惧加强的惊吓。更多研究产生的地图显示,中枢核的输出会影响大脑中涉及恐惧和焦虑症状的其他区域,例如血压升高,出汗,皮肤湿冷,气喘和瞳孔扩张。然而,戴维斯特别感兴趣的是中央核与长期认为相互关联的另一部分amygdale之间的联系,即纹状体末端(BNST)的床核。当药物灭活BNST时,惊恐反应被完全阻断。戴维斯开始解开这两个领域的机制,并发现一种特定的肽,促肾上腺皮质激素释放激素(CRH)“会产生一种看起来非常像恐惧和焦虑的行为的星座”。 - 仅在BNST中作用于受体。他开始测试两个系统在大脑中并行运行的想法:恐惧,持续时间相对较短,由中央核心协调;和焦虑,更加分散和持续,源于BNST。戴维斯提出,认知输入(可能是糟糕的经历和记忆)有助于推动CRH的释放和长期焦虑,包括常见的使人衰弱的恐惧症(恐高症,黑暗)和创伤后应激障碍。研究表明,为了消除这种恐惧,新的“抑制”和学习必须发生。戴维斯最近发现了一种化合物D-环丝氨酸,这种化合物已被证明在旨在消灭恐惧症的心理疗法中非常有前途。 |
课程简介: | Few scientists have charted the grim territory of fear and anxiety with the same doggedness and precision as Michael Davis. Nearly four decades ago, researchers learned that animals, including humans, startle more when fearful. A sudden noise in a dark, creepy alley provokes a greater reaction than in a well-lit room, for instance. That got Davis and his colleagues wondering what neural mechanisms underlie the startle reflex, and how fear plays a part in the response. In his talk, Davis describes the meticulous experiments he and others have conducted over many years. Starting with the fear potentiated startle test -- where animals are trained to pair a stimulus such as light, or sound, with a shock -- researchers began to track the pathways that mediate the response in the nervous system. Using chemical tracers that could follow electrical activity in the brain, Davis found a group of cells in the central nucleus of the amygdala that are critical for fear conditioning. “It was a nice day in the laboratory,” he says. When he knocked out this part of the amygdala with drugs or a lesion, it selectively decreased fear potentiated startle. More studies produced maps showing that outputs of the central nucleus affect other areas of the brain involved in the symptoms of fear and anxiety, such as elevated blood pressure, sweating, clammy skin, panting and pupil dilation. Of particular interest to Davis, though, were the connections between the central nucleus and another part of the amygdale long thought to be interrelated, the bed nucleus of stria terminalis (BNST). When drugs inactivated the BNST, the startle response was completely blocked. Davis began disentangling the mechanisms of these two areas, and found that a specific peptide, corticotrophin releasing hormone (CRH) “produces a constellation of behaviors that look very much like fear and anxiety” -- and acts on receptors only in the BNST. He began to test the idea of two systems acting in parallel in the brain: fear, of relatively short duration, orchestrated by the central nucleus; and anxiety, more diffuse and sustained, originating in the BNST. Davis proposes that cognitive inputs (perhaps bad experiences and memories) help drive the release of CRH and long-term anxiety, including common debilitating phobias (fear of heights, darkness) and post-traumatic stress disorder. Research has shown that to extinguish such fears, new kinds of ‘inhibitory’ learning must take place. Davis recently discovered a compound, D-cycloserine, that has proved extremely promising in psychotherapy aimed at extinguishing phobias. |
关 键 词: | 神经生物学的恐惧; 焦虑和灭绝; 心理治疗 |
课程来源: | 视频讲座网 |
最后编审: | 2020-07-12:yumf |
阅读次数: | 66 |