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调节功能障碍:重度抑郁症中自上而下的前额叶-皮层下神经回路的适得其反的募集

Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression.

作者信息

Johnstone Tom, van Reekum Carien M, Urry Heather L, Kalin Ned H, Davidson Richard J

机构信息

Waisman Laboratory for Brain Imaging and Behavior, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA.

出版信息

J Neurosci. 2007 Aug 15;27(33):8877-84. doi: 10.1523/JNEUROSCI.2063-07.2007.

DOI:10.1523/JNEUROSCI.2063-07.2007
PMID:17699669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6672169/
Abstract

Although depressed mood is a normal occurrence in response to adversity in all individuals, what distinguishes those who are vulnerable to major depressive disorder (MDD) is their inability to effectively regulate negative mood when it arises. Investigating the neural underpinnings of adaptive emotion regulation and the extent to which such processes are compromised in MDD may be helpful in understanding the pathophysiology of depression. We report results from a functional magnetic resonance imaging study demonstrating left-lateralized activation in the prefrontal cortex (PFC) when downregulating negative affect in nondepressed individuals, whereas depressed individuals showed bilateral PFC activation. Furthermore, during an effortful affective reappraisal task, nondepressed individuals showed an inverse relationship between activation in left ventrolateral PFC and the amygdala that is mediated by the ventromedial PFC (VMPFC). No such relationship was found for depressed individuals, who instead show a positive association between VMPFC and amygdala. Pupil dilation data suggest that those depressed patients who expend more effort to reappraise negative stimuli are characterized by accentuated activation in the amygdala, insula, and thalamus, whereas nondepressed individuals exhibit the opposite pattern. These findings indicate that a key feature underlying the pathophysiology of major depression is the counterproductive engagement of right prefrontal cortex and the lack of engagement of left lateral-ventromedial prefrontal circuitry important for the downregulation of amygdala responses to negative stimuli.

摘要

尽管情绪低落是所有人在面对逆境时的正常反应,但易患重度抑郁症(MDD)的人与众不同之处在于,当负面情绪出现时,他们无法有效地调节这种情绪。研究适应性情绪调节的神经基础以及这些过程在MDD中受损的程度,可能有助于理解抑郁症的病理生理学。我们报告了一项功能磁共振成像研究的结果,该研究表明,在非抑郁个体下调负面情绪时,前额叶皮质(PFC)左侧出现激活,而抑郁个体则表现为双侧PFC激活。此外,在一项费力的情感重新评估任务中,非抑郁个体在左腹外侧前额叶皮质和杏仁核的激活之间呈现出一种由腹内侧前额叶皮质(VMPFC)介导的反向关系。而抑郁个体未发现这种关系,相反,他们在VMPFC和杏仁核之间呈现出正相关。瞳孔扩张数据表明,那些花费更多努力重新评估负面刺激的抑郁患者,其杏仁核、脑岛和丘脑的激活更为明显,而非抑郁个体则呈现相反的模式。这些发现表明,重度抑郁症病理生理学的一个关键特征是右侧前额叶皮质的适得其反的参与,以及对杏仁核对负面刺激反应下调很重要的左侧外侧腹内侧前额叶回路的未参与。

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