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Ketamine alters neural processing of facial emotion recognition in healthy men: an fMRI study.

机译:氯胺酮改变健康男人面部情感识别的神经处理:一项功能磁共振成像研究。

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Disruption of facial emotion perception occurs in neuropsychiatric disorders where the expression of emotion is dulled or blunted, for example depersonalization disorder and schizophrenia. It has been suggested that, in the clinical context of emotional blunting, there is a shift in the relative contribution of brain regions subserving cognitive and emotional processing. The non-competitive glutamate receptor antagonist ketamine produces such emotional blunting in healthy subjects. Therefore, we hypothesised that in healthy subjects ketamine would elicit neural responses to emotional stimuli which mimicked those reported in depersonalization disorder and schizophrenia. Thus, we predicted that ketamine would produce reduced activity in limbic and visual brain regions involved in emotion processing, and increased activity in dorsal regions of the prefrontal cortex and cingulate gyrus, both associated with cognitive processing and, putatively, with emotion regulation. Measuring BOLD signal change in fMRI,we examined the neural correlates of ketamine-induced emotional blunting in eight young right-handed healthy men receiving an infusion of ketamine or saline placebo while viewing alternating 30 s blocks of faces displaying fear versus neutral expressions. The normal pattern of neural response occurred in limbic and visual cortex to fearful faces during the placebo infusion. Ketamine abolished this: significant BOLD signal change was demonstrated only in left visual cortex. However, with ketamine, neural responses were demonstrated to neutral expressions in visual cortex, cerebellum and left posterior cingulate gyrus. Emotional blunting may be associated with reduced limbic responses to emotional stimuli and a relative increase in the visual cortical response to neutral stimuli.
机译:在情绪表达迟钝或钝化的神经精神疾病中会发生面部情绪感知中断,例如人格解体障碍和精神分裂症。已经提出,在情感钝化的临床背景下,大脑区域在维护认知和情感加工方面的相对贡献发生了变化。非竞争性谷氨酸受体拮抗剂氯胺酮在健康受试者中产生这种情绪钝化。因此,我们假设在健康的受试者中,氯胺酮会引起对情绪刺激的神经反应,这种反应模仿了人格解体障碍和精神分裂症中的报道。因此,我们预测氯胺酮会降低参与情绪加工的边缘和视觉大脑区域的活动,并增加前额叶皮层和扣带回的背侧区域的活动,这两者都与认知加工有关,并且可能与情绪调节有关。通过测量功能磁共振成像中的大胆信号变化,我们检查了八名右手健康年轻人中氯胺酮引起的情绪钝化的神经相关性,这些男性接受了氯胺酮或生理盐水安慰剂的注入,同时观察了30 s交替显示恐惧和中性表情的面部。在安慰剂输注过程中,神经反应的正常模式发生在边缘和视觉皮层的恐惧面孔上。氯胺酮消除了这一点:仅在左视觉皮层中显示出明显的BOLD信号变化。然而,对于氯胺酮,已证明对视觉皮层,小脑和左后扣带回的中性表达具有神经反应。情绪钝化可能与对情绪刺激的边缘反应减少以及对中性刺激的视觉皮层反应相对增加有关。

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