Loss of sustained activity in the ventromedial prefrontal cortex in response to repeated stress in individuals with early-life emotional abuse: implications for depression vulnerability.
Loss of sustained activity in the ventromedial prefrontal cortex in response to repeated stress in individuals with early-life emotional abuse: implications for depression vulnerability.
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DOI：
10.3389/fpsyg.2013.00320
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发表时间：
2013
影响因子：
3.8
通讯作者：
Smoski MJ
中科院分区：
文献类型：
--
作者：
Wang L;Paul N;Stanton SJ;Greeson JM;Smoski MJ
在早期生活中反复的心理社会压力对行为和神经功能都有显着影响，这两者共同增加了抑郁症的脆弱性。然而，与重复应激相关的神经机制仍不清楚。我们假设，早期生活压力可能会导致认知控制能力降低，以应对反复的压力源，特别是在个人发展适应不良的情绪处理策略，即特质反刍。那些经历过早期生活压力但具有适应性情绪处理（即特质正念）的人可能会表现出相反的模式。使用心算任务诱导轻度压力和正念呼吸任务诱导正念状态，我们通过检查健康年轻男性血液灌注随时间的变化来验证这一假设。我们发现，随着时间的推移，受试者的早期生活压力，特别是情绪虐待，未能维持眶额和腹内侧前额叶皮层（vmPFC）的神经激活。鉴于已知vmPFC在情绪处理过程中调节杏仁核活动，我们随后比较了抑郁易感（具有早期生活压力和高反刍）和弹性（具有早期生活压力和高正念）受试者的vmPFC和杏仁核的灌注。我们发现，抑郁易感受试者增加杏仁核灌注和减少VMPFC灌注在较晚的运行比在较早的压力任务运行。相比之下，抗抑郁的个体表现出相反的模式。我们的研究结果表明，抑郁症易感受试者的vmPFC可能有一个有限的能力，抑制杏仁核激活反复压力随着时间的推移，而在弹性个人的vmPFC可能会迅速适应压力。这项初步研究保证未来的调查，以澄清压力相关的神经活动模式动态识别抑郁症的脆弱性在个人层面上。
Repeated psychosocial stress in early-life has significant impact on both behavior and neural function which, together, increase vulnerability to depression. However, neural mechanisms related to repeated stress remain unclear. We hypothesize that early-life stress may result in a reduced capacity for cognitive control in response to a repeated stressor, particularly in individuals who developed maladaptive emotional processing strategies, namely trait rumination. Individuals who encountered early-life stress but have adaptive emotional processing, namely trait mindfulness, may demonstrate an opposite pattern. Using a mental arithmetic task to induce mild stress and a mindful breathing task to induce a mindful state, we tested this hypothesis by examining blood perfusion changes over time in healthy young men. We found that subjects with early-life stress, particularly emotional abuse, failed to sustain neural activation in the orbitofrontal and ventromedial prefrontal cortex (vmPFC) over time. Given that the vmPFC is known to regulate amygdala activity during emotional processing, we subsequently compared the perfusion in the vmPFC and the amygdala in depression-vulnerable (having early-life stress and high in rumination) and resilient (having early-life stress and high in mindfulness) subjects. We found that depression-vulnerable subjects had increased amygdala perfusion and reduced vmPFC perfusion during the later runs than that during the earlier stressful task runs. In contrast, depression-resilient individuals showed the reverse pattern. Our results indicate that the vmPFC of depression-vulnerable subjects may have a limited capacity to inhibit amygdala activation to repeated stress over time, whereas the vmPFC in resilient individuals may adapt to stress quickly. This pilot study warrants future investigation to clarify the stress-related neural activity pattern dynamically to identify depression vulnerability at an individual level.
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