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Neuroimaging study of placebo analgesia in humans

安慰剂镇痛的神经影像学研究

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Abstract

Placebo has been reported to exert beneficial effects in patients regarding the treatment of pain. Human functional neuroimaging technology can study the intact human brain to elucidate its functional neuroanatomy and the neurobiological mechanism of the placebo effect. Blood flow measurement using functional magnetic resonance imaging and positron emission tomography (PET) has revealed that analgesia is related to decreased neural activities in pain-modulatory brain regions, such as the rostral anterior cingulate cortex (rACC), insula, thalamus, and brainstem including periaqueductal gray (PAG) and ventromedial medulla. The endogenous opioid system and its activation of μ-opioid receptors are thought to mediate the observed effects of placebo. The μ-opioid receptor-selective radiotracer-labeled PET studies show that the placebo effects are accompanied by reduction in activation of opioid neural transmission in pain-sensitive brain regions, including rACC, prefrontal cortex, insula, thalamus, amygdala, nucleus accumbens (NAC) and PAG. Further PET studies with dopamine D2/D3 receptor-labeling radiotracer demonstrate that basal ganglia including NAC are related to placebo analgesic responses. NAC dopamine release induced by placebo analgesia is related to expectation of analgesia. These data indicate that the aforementioned brain regions and neurotransmitters such as endogenous opioid and dopamine systems contribute to placebo analgesia.

摘要

许多文献资料报道了安慰剂对疼痛的镇痛效果。 人体大脑功能影像技术可以在无创伤条件下研究安慰剂镇痛的大脑功能解剖结构及其神经生物学机制。 功能磁共振成像和正电子发射断层扫描(PET)的脑血流测定表明大脑前扣带回喙部(rACC)、 脑岛、 丘脑和脑干的中脑导水管周围灰质(PAG)及延髓头端腹侧部的神经兴奋性降低与安慰剂镇痛调节有关。 内源性吗啡肽系统及激活吗啡肽μ受体参与安慰剂的镇痛作用。 吗啡肽μ受体标记的PET影像研究提示安慰剂镇痛伴随着疼痛相关大脑部位(如rACC、 前额叶皮层、 脑岛、 丘脑、 杏仁核、 伏隔核、 PAG 等)中内源性吗啡肽活性的降低。 此外, 标记多巴胺D2/D3 受体的PET 实验证明基底核包括伏隔核的多巴胺活性与安慰剂镇痛相关。 安慰剂镇痛引起的伏隔核的多巴胺释放与安慰剂 期待相关。 以上结果提示上述大脑区域和内源性吗啡肽及多巴胺在安慰剂镇痛方面有重要作用。

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Correspondence to Yun-Hai Qiu  (秋云海).

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Qiu, YH., Wu, XY., Xu, H. et al. Neuroimaging study of placebo analgesia in humans. Neurosci. Bull. 25, 277–282 (2009). https://doi.org/10.1007/s12264-009-0907-2

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