Chase M H, Morales F R
Science. 1983 Sep 16;221(4616):1195-8. doi: 10.1126/science.6310749.
A striking paradox of the rapid eye movement periods of active sleep, which are typically characterized by the exacerbation of somatomotor atonia, is the occurrence of muscle twitches and jerks. The purpose of this study was to examine the specific motoneuron membrane potential processes responsible for these myoclonic patterns of activity. In lumbar motoneurons, examined intracellularly in the cat prepared for long-term study, these processes consisted of recurrent depolarizing membrane potential shifts and spontaneous action potentials that were either full-sized or of partial amplitude. In addition, the invasion of antidromically induced spikes into the soma was often blocked. Hyperpolarizing potentials were evident in the intervals between spontaneous spikes. Hyperpolarization was also observed immediately before depolarization and spike activity, in contrast to the gradual depolarization of the motoneuron membrane potential that always occurred during wakefulness. Thus, during rapid eye movement periods, in conjunction with muscle twitches and jerks, a strong excitatory input is superimposed on a background of inhibitory input. The unique patterns of membrane potential change that arise thus seem to result from the simultaneous coactivation of excitatory and inhibitory processes.
快速眼动期的主动睡眠存在一个显著的矛盾现象,该时期通常以躯体运动性肌张力缺失加剧为特征,却会出现肌肉抽搐和痉挛。本研究的目的是探究导致这些肌阵挛性活动模式的特定运动神经元膜电位过程。在为长期研究而准备的猫身上,对其腰段运动神经元进行细胞内检测,这些过程包括反复的去极化膜电位变化以及全幅度或部分幅度的自发动作电位。此外,逆向诱导的尖峰侵入胞体的情况常常受阻。在自发尖峰之间的间隔期,超极化电位很明显。与清醒时运动神经元膜电位总是逐渐去极化不同,在去极化和尖峰活动之前也观察到了超极化。因此,在快速眼动期,伴随着肌肉抽搐和痉挛,强烈的兴奋性输入叠加在抑制性输入的背景之上。由此产生的独特膜电位变化模式似乎是由兴奋性和抑制性过程的同时共同激活导致的。