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慢睡眠振荡、节律性K复合波及其阵发性发展。

Slow sleep oscillation, rhythmic K-complexes, and their paroxysmal developments.

作者信息

Steriade M, Amzica F

机构信息

Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Québec, Canada.

出版信息

J Sleep Res. 1998;7 Suppl 1:30-5. doi: 10.1046/j.1365-2869.7.s1.4.x.

Abstract

This paper presents the relations between the slow (< 1 Hz) oscillation (characterizing the activity of corticothalamic networks during quiescent sleep in cats and humans), sleep K-complexes, and some paroxysmal developments of sleep patterns. At the cellular level, the slow oscillation is built up by rhythmic membrane depolarizations and hyperpolarizations of cortical neurons. The EEG expression of this activity is marked by periodic K-complexes which reflect neuronal excitation. The slow oscillation triggers, groups and synchronizes other sleep rhythms, such as thalamically generated spindles as well as thalamically and cortically generated delta oscillations. We discuss the distinctness of the slow (< 1 Hz) and delta (1-4 Hz) oscillations. We also show that the slow cortical oscillation underlies the onset of spike-wave seizures during sleep by transforming the periodic K-complexes into recurrent paroxysmal spike-wave complexes.

摘要

本文介绍了慢波(<1Hz)振荡(表征猫和人类静息睡眠期间皮质丘脑网络的活动)、睡眠K复合波以及睡眠模式的一些阵发性变化之间的关系。在细胞水平上,慢波振荡由皮质神经元有节奏的膜去极化和超极化构成。这种活动的脑电图表现以周期性K复合波为特征,其反映了神经元兴奋。慢波振荡触发、分组并同步其他睡眠节律,如丘脑产生的纺锤波以及丘脑和皮质产生的δ振荡。我们讨论了慢波(<1Hz)和δ波(1-4Hz)振荡的差异。我们还表明,睡眠期间皮质慢波振荡通过将周期性K复合波转变为反复出现的阵发性棘波-慢波复合波,构成了棘波-慢波癫痫发作的起始机制。

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