Glenn L L, Dement W C
Brain Res. 1982 Jul 8;243(1):11-23. doi: 10.1016/0006-8993(82)91116-7.
Electrophysiological antecedents to electromyogram pauses of NREM sleep were studied intracellularly in hindlimb motoneurons. Phasic-event-related hyperpolarizing potentials (PRHP) were 0.2-7.1 mV in amplitude and 9-90 ms in duration, and coincided with dorsal neck EMG pauses and PGO waves. Motoneurons, if spontaneously discharging, were silenced during PRHPs. The discharge rate of spike trains elicited by depolarizing current reduced during PRHPs. Membrane conductance measurements indicated that PRHPs did not arise simply from soma inhibition but from either presynaptic inhibition or conductance changes in electrically-remote dendrites. EMG pauses, which normally occur spontaneously, could be evoked by stimulation of low threshold fibers in peripheral nerves. PRHPs were most prevalent in REM sleep. We concluded that EMG pauses are generated by the same cholinergic brainstem mechanism that generates spino-bulbo-spinal presynaptic inhibition of group Ia afferents. The pauses resemble the inhibitory phase of startle responses, providing evidence for the hypothesis that startle responses are spontaneously elicited in NREM and REM sleep.
我们在下肢运动神经元中进行细胞内研究,以探究非快速眼动睡眠肌电图停顿的电生理前体。相位事件相关超极化电位(PRHP)的幅度为0.2 - 7.1 mV,持续时间为9 - 90毫秒,与颈背肌电图停顿和PGO波同时出现。运动神经元如果自发放电,在PRHP期间会沉默。去极化电流引发的动作电位序列的放电率在PRHP期间降低。膜电导测量表明,PRHP并非仅仅源于胞体抑制,而是源于突触前抑制或电远程树突中的电导变化。通常自发出现的肌电图停顿可通过刺激外周神经中的低阈值纤维诱发。PRHP在快速眼动睡眠中最为普遍。我们得出结论,肌电图停顿是由与产生Ia类传入纤维的脊髓 - 延髓 - 脊髓突触前抑制相同的胆碱能脑干机制产生的。这些停顿类似于惊吓反应的抑制阶段,为惊吓反应在非快速眼动和快速眼动睡眠中自发引发的假说提供了证据。