Facilitation of Extinction of Conditioned Fear by D-Cycloserine
Facilitation of Extinction of Conditioned Fear by D-Cycloserine
复制标题
D-环丝氨酸促进条件性恐惧的消除
DOI：
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
B. Rothbaum
中科院分区：
文献类型：
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作者：
M. Davis;Karyn M. Myers;K. Ressler;B. Rothbaum
过度恐惧和焦虑是创伤后应激障碍(PTSD)和恐惧症等疾病的特征，被认为反映了控制条件性恐惧的发展和减少的神经系统的异常。条件性恐惧可以通过一种称为消退的过程来抑制，在这种过程中，在没有令人厌恶的事件的情况下，反复暴露于令人恐惧的刺激下，会导致对该刺激的恐惧反应逐渐减少。像条件性恐惧学习一样，消退依赖于大脑中称为杏仁核的部分中的一种特定蛋白质(N-甲基-D-天冬氨酸或NMDA受体)。阻断这种受体可以阻止这种受体的消亡，而用一种名为D-环丝氨酸的药物改善这种受体的活性可以加速大鼠的消亡。由于基于暴露的人类恐惧障碍心理治疗在几个方面类似于灭绝，我们调查了D-环丝氨酸是否可能有助于人类患者消除恐惧。与动物实验室的发现一致，接受D-环丝氨酸治疗的患者比接受安慰剂治疗的对照组从基于暴露的心理治疗中受益更多。虽然非常初步，但这些数据为认知增强剂在心理治疗中的使用提供了初步支持，并证明了啮齿动物的临床前研究可以对人类产生直接好处。
Excessive fear and anxiety are characteristic of disorders such as post-traumatic stress disorder (PTSD) and phobias and are believed to reflect abnormalities in neural systems governing the development and reduction of conditioned fear. Conditioned fear can be suppressed through a process known as extinction, in which repeated exposure to a feared stimulus in the absence of an aversive event leads to a gradual reduction in the fear response to that stimulus. Like conditioned fear learning, extinction is dependent on a particular protein (the N-methyl-D-aspartate or NMDA receptor) in a part of the brain called the amygdala. Blockade of this receptor blocks extinction and improving the activity of this receptor with a drug called D-cycloserine speeds up extinction in rats. Because exposure-based psychotherapy for fear disorders in humans resembles extinction in several respects, we investigated whether D-cycloserine might facilitate the loss of fear in human patients. Consistent with findings from the animal laboratory, patients receiving D-cycloserine benefited more from exposure-based psychotherapy than did placebo-treated controls. Although very preliminary, these data provide initial support for the use of cognitive enhancers in psychotherapy and demonstrate that preclinical studies in rodents can have direct benefits to humans.
影响因子：
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作者：
Ressler, KJ;Rothbaum, BO;Davis, M
通讯作者：
Davis, M