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快速眼动睡眠期相性事件孤立发作和成簇发作期间后肢伸肌α运动神经元的膜电位和输入电阻

Membrane potential and input resistance in alpha motoneurons of hindlimb extensors during isolated and clustered episodes of phasic events in REM sleep.

作者信息

Glenn L L, Dement W C

出版信息

Brain Res. 1985 Jul 22;339(1):79-86. doi: 10.1016/0006-8993(85)90623-7.

DOI:10.1016/0006-8993(85)90623-7
PMID:2992699
Abstract

The function of motoneurons during the phasic events of REM sleep was investigated in cats. The membrane potential, synaptic activity, input resistance and rheobase were measured in hindlimb extensor motoneurons during periods of concentrated phasic events (Type II) in REM sleep in undrugged, minimally restrained cats. During Type II episodes in REM sleep, motoneurons depolarized 3 mV on the average, reduced in input resistance by 20%, and had distinct increases in spontaneous synaptic activity, as compared with periods of REM sleep between episodes (i.e. Type I). This constellation of properties is explained by increased frequencies of both unitary EPSPs and IPSPs in motoneurons. Myoclonic jerks in Type II episodes do not appear to arise because of a temporary withdrawal of the tonic motoneuron inhibition found in REM sleep. Instead, large increases in excitatory synaptic activity overcome the inhibition, giving rise to motoneuron discharges.

摘要

在猫身上研究了快速眼动睡眠阶段事件期间运动神经元的功能。在未用药、轻度约束的猫处于快速眼动睡眠集中阶段事件(II型)期间,测量了后肢伸肌运动神经元的膜电位、突触活动、输入电阻和基强度。与快速眼动睡眠事件之间的阶段(即I型)相比,在快速眼动睡眠的II型发作期间,运动神经元平均去极化3 mV,输入电阻降低20%,并且自发突触活动明显增加。运动神经元中单位兴奋性突触后电位和抑制性突触后电位频率的增加解释了这种特性组合。II型发作中的肌阵挛性抽搐似乎并非由于快速眼动睡眠中发现的紧张性运动神经元抑制的暂时解除而产生。相反,兴奋性突触活动的大幅增加克服了抑制作用,导致运动神经元放电。

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