Fung Simon J, Chase Michael H
VA Greater Los Angeles Healthcare System, Los Angeles, CA: Websciences International, Los Angeles, CA.
VA Greater Los Angeles Healthcare System, Los Angeles, CA: Websciences International, Los Angeles, CA: Department of Physiology, UCLA School of Medicine, Los Angeles, CA.
Sleep. 2015 Jan 1;38(1):139-46. doi: 10.5665/sleep.4340.
Hypoglossal motoneurons were recorded intracellularly to determine whether postsynaptic inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep.
Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined.
During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep.
We conclude that hypoglossal motoneurons are postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated postsynaptic inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
对舌下运动神经元进行细胞内记录，以确定快速眼动（REM）睡眠期间舌肌弛缓是由突触后抑制还是去易化作用引起的。
在猫处于清醒、非快速眼动（NREM）睡眠和REM睡眠状态时，对经逆向鉴定的舌下运动神经元的动作电位和阈下膜电位活动进行细胞内记录。在舌下神经周围放置袖带电极以逆向激活舌下运动神经元。确定舌下运动神经元膜电位、自发放电、突触后电位和基强度的状态依赖性变化。
在安静清醒和NREM睡眠期间，舌下运动神经元表现出自发性重复放电。从NREM睡眠过渡到REM睡眠时，重复放电停止，膜电位开始超极化；最大超极化（10.5 mV）在整个REM睡眠期间持续存在。在REM睡眠期间，基强度显著增加，同时伴有大量高幅度抑制性突触后电位（IPSPs），在细胞内注入氯离子后这些电位被逆转。后一结果表明它们是由甘氨酸介导的；清醒或NREM睡眠期间不存在IPSPs。
我们得出结论，在自然发生的REM睡眠期间，舌下运动神经元受到突触后抑制；未观察到去易化作用的证据。数据还表明，甘氨酸受体介导的舌下运动神经元突触后抑制在REM睡眠期间促进舌肌弛缓中起关键作用。
