Psychosocial stress reversibly disrupts prefrontal processing and attentional control
Psychosocial stress reversibly disrupts prefrontal processing and attentional control
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DOI：
10.1073/pnas.0807041106
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发表时间：
2009-01-20
影响因子：
11.1
通讯作者：
Casey, B. J.
中科院分区：
文献类型：
--
作者：
Liston, C.;McEwen, B. S.;Casey, B. J.
人们对慢性应激的长期神经生物学后遗症知之甚少，这种后遗症使易感患者容易受到影响前额叶皮质(PFC)的神经精神疾病的影响。动物模型和人类神经成像实验提供了互补的见解，但将两者结合起来的努力往往因为在不相关的研究和完全不同的设计之间进行比较所固有的局限性而变得复杂。从我们已经显示PFC功能可逆中断的啮齿动物模型中，我们发现心理社会应激导致人类PFC功能的行为和功能磁共振成像(FMRI)测量中的长期但可逆的损害。20名健康的成年人，暴露在1个月的心理社会压力下，通过有效的评定量表确认，在执行依赖于PFC的注意力转移任务时进行扫描。一个月后，他们在压力减轻一段时间后返回进行第二次扫描，并将他们的表现与两次扫描、匹配的低压力对照组进行比较。心理社会压力选择性地损害了注意力控制，并破坏了额顶网络内调节注意力转移的功能连接。这些影响是可逆的：在压力减轻一个月后，相同的受试者与对照组没有显著差异。这些结果突显了健康受试者PFC网络的可塑性，并提出了一种机制，即可塑性中断可能导致易感个体的应激相关神经精神疾病的认知障碍。
Relatively little is known about the long-term neurobiological sequelae of chronic stress, which predisposes susceptible patients to neuropsychiatric conditions affecting the prefrontal cortex (PFC). Animal models and human neuroimaging experiments provide complementary insights, yet efforts to integrate the two are often complicated by limitations inherent in drawing comparisons between unrelated studies with disparate designs. Translating from a rodent model of chronic stress where we have shown reversible disruption of PFC function, we show that psychosocial stress induces long-lasting but reversible impairments in behavioral and functional magnetic resonance imaging (fMRI) measures of PFC function in humans. Twenty healthy adults, exposed to 1 month of psychosocial stress, confirmed by a validated rating scale, were scanned while performing a PFC-dependent attention-shifting task. One month later, they returned for a second scanning session after a period of reduced stress, and their performance was compared with a twice-scanned, matched group of low-stress controls. Psychosocial stress selectively impaired attentional control and disrupted functional connectivity within a frontoparietal network that mediates attention shifts. These effects were reversible: after one month of reduced stress, the same subjects showed no significant differences from controls. These results highlight the plasticity of PFC networks in healthy human subjects and suggest one mechanism by which disrupted plasticity may contribute to cognitive impairments characteristic of stress-related neuropsychiatric conditions in susceptible individuals.