Cantero Jose L, Atienza Mercedes, Salas Rosa M, Dominguez-Marin Elena
Laboratory of Sleep and Cognition, 41005 Seville, Spain.
J Neurosci. 2002 Jun 1;22(11):4702-8. doi: 10.1523/JNEUROSCI.22-11-04702.2002.
Evidence suggests that sleep homeostasis is not only dependent on duration of previous wakefulness but also on experience- and/or use-dependent processes. Such homeostatic mechanisms are reflected by selective increases in the duration of a sleep stage, modifications to electrophysiological-metabolic brain patterns in specific sleep states, and/or reactivation to neuronal ensembles in subsequent sleep periods. Use-dependent sleep changes, apparently different from those changes caused by memory consolidation processes, are thought to reflect neuronal restoration processes after the sustained exposure to stimulation during the preceding wakefulness. In the present study, we investigated changes in the brain electrical activity pattern during human sleep after 6 hr of continuous auditory stimulation during previous wakefulness. Poststimulation nights showed a widespread increase of spectral power within the alpha (8-12 Hz) and sleep spindle (12-15 Hz) frequency range during slow-wave sleep (SWS) compared with the baseline night. This effect was mainly attributable to an enhanced EEG amplitude rather than an increase of oscillations, except for temporal (within alpha and sleep spindles) and parietal regions (within sleep spindles) in which both parameters contributed equally to the increase of spectral energy. Power increments were accompanied by a strengthening of the coherence between fronto-temporal cortical regions within a broad frequency range during SWS but to the detriment of the coherence between temporal and parieto-occipital areas, suggesting underlying compensatory mechanisms between temporal and other cortical regions. In both cases, coherence was built up progressively across the night, although no changes were observed within each SWS period. No electrophysiological changes were found in rapid eye movement sleep. These results point to SWS as a critical brain period for correcting the cortical synaptic imbalance produced by the predominant use of specific neuronal populations during the preceding wakefulness, as well as for synaptic reorganization after prolonged exposure to a novel sensory experience.
有证据表明,睡眠稳态不仅取决于先前清醒的时长,还取决于与经验和/或使用相关的过程。这种稳态机制表现为睡眠阶段时长的选择性增加、特定睡眠状态下脑电生理代谢模式的改变,以及/或者在后续睡眠期对神经元群的重新激活。与记忆巩固过程所引起的变化明显不同,与使用相关的睡眠变化被认为反映了在前述清醒期间持续暴露于刺激后神经元的恢复过程。在本研究中,我们调查了在前述清醒期间连续6小时听觉刺激后人类睡眠期间脑电活动模式的变化。与基线夜晚相比,刺激后夜晚在慢波睡眠(SWS)期间,α波(8 - 12赫兹)和睡眠纺锤波(12 - 15赫兹)频率范围内的频谱功率普遍增加。这种效应主要归因于脑电图振幅的增强,而非振荡的增加,但颞叶(α波和睡眠纺锤波范围内)和顶叶区域(睡眠纺锤波范围内)除外,这两个区域的这两个参数对频谱能量增加的贡献相同。功率增加伴随着慢波睡眠期间广泛频率范围内额颞叶皮质区域之间连贯性的增强,但颞叶与颞枕叶区域之间的连贯性则降低了,这表明颞叶与其他皮质区域之间存在潜在的补偿机制。在这两种情况下,连贯性在整个夜晚逐渐增强,尽管在每个慢波睡眠期内未观察到变化。在快速眼动睡眠中未发现电生理变化。这些结果表明,慢波睡眠是纠正先前清醒期间特定神经元群过度使用所产生的皮质突触失衡以及长时间暴露于新的感觉体验后进行突触重组的关键脑期。