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首页> 外文期刊>Journal of Neurophysiology >The motor inhibitory system operating during active sleep is tonically suppressed by GABAergic mechanisms during other states.
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The motor inhibitory system operating during active sleep is tonically suppressed by GABAergic mechanisms during other states.

机译：在其他状态下，GABA能机制在运动性睡眠期间运行的运动抑制系统在声调上受到抑制。

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The present study was undertaken to explore the neuronal mechanisms responsible for muscle atonia that occurs after the microinjection of bicuculline into the nucleus pontis oralis (NPO). Specifically, we wished to test the hypothesis that motoneurons are postsynaptically inhibited after the microinjection of bicuculline into the NPO and determine whether the inhibitory mechanisms are the same as those that are utilized during naturally occurring active (rapid eye movement) sleep. Accordingly, intracellular records were obtained from lumbar motoneurons in cats anesthetized with alpha-chloralose before and during bicuculline-induced motor inhibition. The microinjection of bicuculline into the NPO resulted in a sustained reduction in the amplitude of the spinal cord Ia-monosynaptic reflex. In addition, lumbar motoneurons exhibited significant changes in their electrophysiological properties [i.e., a decrease in input resistance and membrane time constant, a reduction in the amplitude of the action potential's afterhyperpolarization (AHP) and an increase in rheobase]. Discrete, large-amplitude inhibitory postsynaptic potentials (IPSPs) were also observed in high-gain recordings from lumbar motoneurons. These potentials were comparable to those that are only present during the state of naturally occurring active sleep. Furthermore, stimulation of the medullary nucleus reticularis gigantocellularis evoked a large-amplitude IPSP in lumbar motoneurons after, but never prior to, the injection of bicuculline; this reflects the pattern of motor responses that occur in conjunction with the phenomenon of "reticular response-reversal." The preceding changes in the electrophysiological properties of motoneurons, as well as the development of active sleep-specific IPSPs, indicate that lumbar motoneurons are postsynaptically inhibited following the intrapontine administration of bicuculline in a manner that is comparable to that which occurs spontaneously during the atonia of active sleep. The present results support the conclusion that the brain stem-spinal cord inhibitory system, which is responsible for motor inhibition during active sleep, can be activated by the injection of bicuculline into the NPO. These data suggest that the active sleep-dependent motor inhibitory system is under constant GABAergic inhibitory control, which is centered in the NPO. Thus during wakefulness and quiet sleep, the glycinergically mediated postsynaptic inhibition of motoneurons is prevented from occurring due to GABAergic mechanisms.
机译：进行本研究，以探索负责将双小分子显微注射入舟状核（NPO）后发生肌肉肌萎缩的神经元机制。具体而言，我们希望检验以下假设：在将双小分子显微注射到NPO中后，运动神经元被突触后抑制，并确定抑制机制是否与自然活跃（快速眼动）睡眠中使用的抑制机制相同。因此，在双小分子诱导的运动抑制之前和期间，从用α-氯醛麻醉的猫的腰部运动神经元获得了细胞内记录。将比库林微注射到NPO中导致脊髓Ia-单突触反射幅度的持续降低。此外，腰运动神经元在其电生理特性方面表现出显着变化[即，输入电阻和膜时间常数的降低，动作电位的超极化后（AHP）幅度的降低和流变碱的增加]。腰部运动神经元的高增益记录中也观察到离散的大振幅抑制性突触后电位（IPSP）。这些潜力与仅在自然活动睡眠状态下才有的潜力相当。此外，在注射双瓜氨酸后但从未在此之前，刺激了网状巨大神经髓质在腰部运动神经元中引起了大幅度的IPSP。这反映了伴随“网状反应-逆转”现象而发生的运动反应模式。先前运动神经元的电生理特性的变化，以及活动性睡眠特异性IPSP的发展，表明腰椎运动神经元在脑桥下给药双小分子后被突触后抑制的方式与自发性心房颤动自发发生的方式相当。积极睡眠。目前的结果支持这样的结论，即在主动睡眠期间负责运动抑制的脑干-脊髓抑制系统可以通过将双小环素注射到NPO中来激活。这些数据表明，主动睡眠依赖性运动抑制系统处于恒定的GABA能抑制控制之下，该控制以NPO为中心。因此，在清醒和安静的睡眠中，由于GABA能机制，防止了糖原介导的运动神经元的突触后抑制。

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