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睡眠剥夺后编码过程中皮层表象的退化。

Degradation of cortical representations during encoding following sleep deprivation.

机构信息

Centre for Cognitive Neuroscience, Duke-NUS Medical School, 8 College Roadø, Singapore 169857, Republic of Singapore; NUS Graduate School for Integrative Sciences & Engineering, 28 Medical Drive, Singapore 117456, Republic of Singapore.

Centre for Cognitive Neuroscience, Duke-NUS Medical School, 8 College Roadø, Singapore 169857, Republic of Singapore.

出版信息

Neuroimage. 2017 Jun;153:131-138. doi: 10.1016/j.neuroimage.2017.01.080. Epub 2017 Feb 2.

Abstract

A night of total sleep deprivation (TSD) reduces task-related activation of fronto-parietal and higher visual cortical areas. As this reduction in activation corresponds to impaired attention and perceptual processing, it might also be associated with poorer memory encoding. Related animal work has established that cortical columns stochastically enter a 'down' state in sleep deprivation, leading to predictions that neural representations are less stable and distinctive following TSD. To test these predictions participants incidentally encoded scene images while undergoing fMRI, either during rested wakefulness (RW) or after TSD. In scene-selective PPA, TSD reduced stability of neural representations across repetition. This was accompanied by poorer subsequent memory. Greater representational stability benefitted subsequent memory in RW but not TSD. Even for items subsequently recognized, representational distinctiveness was lower in TSD, suggesting that quality of encoding is degraded. Reduced representational stability and distinctiveness are two novel mechanisms by which TSD can contribute to poorer memory formation.

摘要

一夜的完全睡眠剥夺(TSD)会降低额顶和更高视觉皮层区域的任务相关激活。由于这种激活的减少对应于注意力和感知处理受损,它也可能与较差的记忆编码有关。相关的动物研究已经证实,皮质柱在睡眠剥夺时随机进入“关闭”状态,这导致预测神经表示在 TSD 后不太稳定和独特。为了验证这些预测,参与者在进行 fMRI 时偶然地对场景图像进行编码,要么在休息清醒(RW)时,要么在 TSD 后。在场景选择性 PPA 中,TSD 降低了神经表示在重复过程中的稳定性。这伴随着较差的后续记忆。在 RW 中,更大的表示稳定性有利于后续记忆,但在 TSD 中则不然。即使是随后被识别的项目,在 TSD 中的表示独特性也较低,这表明编码质量下降。表示稳定性和独特性降低是 TSD 导致较差记忆形成的两个新机制。

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