Regional pattern of metabolic activation is reflected in the sleep EEG after sleep deprivation combined with unilateral whisker stimulation in mice
Regional pattern of metabolic activation is reflected in the sleep EEG after sleep deprivation combined with unilateral whisker stimulation in mice
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DOI：
10.1111/j.1460-9568.2004.03583.x
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发表时间：
2004-09
影响因子：
3.4
通讯作者：
V. Vyazovskiy;E. Welker;J. Fritschy;I. Tobler
中科院分区：
文献类型：
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作者：
V. Vyazovskiy;E. Welker;J. Fritschy;I. Tobler
睡眠剥夺（SD）后睡眠期间EEG慢波活动（SWA）的区域差异可能是皮质区代谢活化差异的结果。我们研究了小鼠SD后局部EEG动力学与2-脱氧葡萄糖（DG）摄取之间的关系。6小时的SD与丰富环境中的自然单侧胡须刺激相结合，以选择性地激活桶皮质和运动区。正如预期的那样，在SD后立即在桶状皮质中发现了2-DG摄取的半球间不对称性。为了测试睡眠是否有助于恢复不对称性，刺激之后是不受干扰的睡眠或额外的SD。这种不对称性在恢复睡眠后消失了，但在没有刺激的额外清醒期后也消失了。此外，SD后即刻初级运动皮层和压后区的相对2-DG摄取量显著高于额外睡眠或觉醒后，而两组之间没有其他区域差异。在非快速眼动睡眠期间，胡须刺激引起受刺激半球的EEG SWA比对照半球更大的增加，这种增加持续10 h。在一个半球内，SWA的初始增加额高于顶叶派生。我们得出结论，睡眠期间的区域SWA差异是使用依赖性的，可能与之前清醒期间的区域代谢模式有关。然而，局部代谢的恢复并不依赖于睡眠，也不直接反映在睡眠期间SWA的变化上。
Regional differences in EEG slow wave activity (SWA) during sleep after sleep deprivation (SD) may be a consequence of differential metabolic activation of cortical areas. We investigated the relationship between the regional EEG dynamics and 2‐deoxyglucose (DG) uptake after SD in mice. Six hours' SD were combined with natural unilateral whisker stimulation in an enriched environment to selectively activate the barrel cortex and motor areas. As expected, an interhemispheric asymmetry of 2‐DG uptake was found in the barrel cortex immediately after SD. To test whether sleep contributes to recovery of the asymmetry, the stimulation was followed by either undisturbed sleep or by an additional SD. The asymmetry vanished after recovery sleep but also after the additional period of wakefulness without stimulation. In addition, relative 2‐DG uptake in the primary motor cortex and retrosplenial area was significantly higher immediately after the SD than after the additional sleep or wakefulness, whereas no other region differed between the groups. Whisker stimulation elicited a greater increase in EEG SWA during non rapid eye movement sleep in the stimulated hemisphere than in the control hemisphere; this increase lasted for 10 h. Within a hemisphere, the initial increase in SWA was higher in the frontal than in the parietal derivation. We conclude that the regional SWA differences during sleep are use‐dependent and may be related to the regional pattern of metabolism during the previous waking episode. However, the regional metabolic recovery is not dependent on sleep, and is not directly reflected in changes in SWA during sleep.