Prefrontal Markers and Cognitive Performance Are Dissociated during Progressive Dopamine Lesion

Prefrontal Markers and Cognitive Performance Are Dissociated during Progressive Dopamine Lesion
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进行性多巴胺损伤期间前额叶标记和认知表现分离

DOI:
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发表时间:
2016
期刊:
影响因子:
9.8
通讯作者:
E. Procyk
E. Procyk
中科院分区:
生物学1区
文献类型:
--
作者:
Charles R. E. Wilson;J. Vezoli;Frederic M. Stoll;Maïlys C M Faraut;V. Leviel;K. Knoblauch;E. Procyk

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多巴胺被认为直接影响表现监控和认知控制的神经生理机制,这两个过程在适应行为的产生中有着重要的联系。多巴胺水平的变化也被认为会引起几种神经和精神疾病的认知变化。但是,这一系统的工作模式作为一个整体仍然未经测试。具体来说,尽管许多研究人员认为多巴胺水平的变化会改变神经生理机制及其在额叶皮层的标志物,进而导致认知变化,但这一因果链需要得到验证。在非人类灵长类动物进行性多巴胺能损伤过程中,使用额叶神经生理学标记物的纵向记录超过数月,我们提供的数据无法支持多巴胺、额叶功能和认知之间的简单相互作用。反馈电位,这是性能监测信号,有时被认为是驱动成功的控制,停止分化反馈价在病变结束时,就在临床运动阈值。相比之下,认知控制性能和认知控制的β振荡标记物未受到损害。在整个多巴胺损伤过程中,这些指标的不同动态表明,它们并不都是以相同的方式由多巴胺驱动的。这些动力学也表明,一个复杂的非线性机制集是从事在大脑中的进行性多巴胺病变的反应。这些结果质疑了从多巴胺到额叶生理学再到认知的直接因果链。这意味着认知功能的生物标志物不能直接预测多巴胺的损失。
Dopamine is thought to directly influence the neurophysiological mechanisms of both performance monitoring and cognitive control—two processes that are critically linked in the production of adapted behaviour. Changing dopamine levels are also thought to induce cognitive changes in several neurological and psychiatric conditions. But the working model of this system as a whole remains untested. Specifically, although many researchers assume that changing dopamine levels modify neurophysiological mechanisms and their markers in frontal cortex, and that this in turn leads to cognitive changes, this causal chain needs to be verified. Using longitudinal recordings of frontal neurophysiological markers over many months during progressive dopaminergic lesion in non-human primates, we provide data that fail to support a simple interaction between dopamine, frontal function, and cognition. Feedback potentials, which are performance-monitoring signals sometimes thought to drive successful control, ceased to differentiate feedback valence at the end of the lesion, just before clinical motor threshold. In contrast, cognitive control performance and beta oscillatory markers of cognitive control were unimpaired by the lesion. The differing dynamics of these measures throughout a dopamine lesion suggests they are not all driven by dopamine in the same way. These dynamics also demonstrate that a complex non-linear set of mechanisms is engaged in the brain in response to a progressive dopamine lesion. These results question the direct causal chain from dopamine to frontal physiology and on to cognition. They imply that biomarkers of cognitive functions are not directly predictive of dopamine loss.
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