压倒性的连贯,由独立实验室开发的综合数据体,几十年来,使用细胞内记录结合神经递质和拮抗剂的细胞间微离子电渗注射,最终证明了突触后抑制,由甘氨酸介导,是关键和充分的过程,完全解释了在REM睡眠的强直和阶段性期间运动神经元放电的抑制。这些研究,其中许多是完好无损地进行的,自然睡觉,成年动物,消除使用减少的潜在解释性并发症,体外切片或甚至完整的体内制剂;它们还提供微透析不可能的分辨率水平。另一方面,当在三叉神经运动池和相邻区域中输注物质混合物两到四个小时时,预计将获得无法解释的非生理结果,特别是当数千种细胞上的受体被激活时,这些受体专门负责促进三叉神经运动神经元的觉醒相关功能。因为如此大的区域中的受体被Brooks和Peever透析的物质不加区别地激活,显然不可能得出结论,EMG活性的任何变化仅仅是由于参与状态依赖性过程的α运动神经元上受体的激活.此外,因为Brooks和Peever获得的结果不能归因于任何特定类型的受体,突触过程,或细胞类型,无法将他们的发现与细胞内研究获得的数据进行比较.尽管如此,他们实验的技术执行质量极高。鉴于布鲁克斯和皮弗的这种明显的力量,不幸的是,他们没有利用一种技术来获得有意义的数据,如细胞内记录。事实上,产生了一种制剂,在这种制剂中,可以在自然发生的睡眠和觉醒状态下记录细胞内和细胞间排出物质,在两年的时间里,特别是为了避免Brooks和Peever采用的微透析技术固有的问题。总之,在清醒的时候,在三叉神经运动核及其附近的许多神经元元件上的许多受体通常以高度调节的序列被激活,这取决于正在进行的特定行为,比如发声,咬人,咀嚼,吞咽,等。另一方面,在REM睡眠期间,只有三叉神经运动神经元上的受体,参与状态相关的控制过程,很兴奋。这些受体已被鉴定为甘氨酸能,并已显示被激活,单突触,通过网状巨细胞核区域的投影。因此,Brooks和Peever没有理由声称一个未知的“生化底物”是引起快速眼动睡眠中失去障碍的原因,他们也没有提供任何数据或理由不继续相信他们最初陈述的真实性,反映了“躯体运动神经元的甘氨酸能抑制是快速眼动睡眠中姿势肌张力丧失的原因”的共识。
An overwhelmingly coherent, integrated body of data developed by independent laboratories, over many decades, using intracellular recording in conjunction with the juxtacellular microiontophoretic ejection of neurotransmitters and antagonists, demonstrates conclusively that postsynaptic inhibition, mediated by glycine, is the critical and sufficient process that completely accounts for the suppression of motoneuron discharge during the tonic and phasic periods of REM sleep. These studies, many of which were conducted in intact, naturally sleeping, adult animals, eliminate potential interpretive complications that arise using reduced, in vitro slice or even intact in vivo preparations; they also provide for levels of resolutions that are not possible with microdialysis. On the other hand, when infusing a cocktail of substances for two to four hours into the trigeminal motor pool and adjacent regions, it is to be expected that uninterpretable and nonphysiological results would be obtained, especially when thousands of receptors on thousands of cells that are exclusively responsible for promoting waking-related functions of trigeminal motoneurons are activated. Because receptors in such a large region were indiscriminately activated by substances that Brooks and Peever dialyzed, it is clearly impossible to conclude that any change in EMG activity was due only to the activation of receptors on alpha motoneurons that are involved in state-dependent processes. In addition, because the results that Brooks and Peever obtained cannot be attributed to any specific class of receptors, synaptic process, or cell type, it is not possible to compare their findings with data obtained from intracellular studies. The preceding notwithstanding, the technical execution of their experiments was of an extremely high quality. Given this obvious strength of Brooks and Peever, it is unfortunate that they did not utilize a technique that would have allowed them to obtain meaningful data, such as intracellular recording. In point of fact, the generation of a preparation in which it is possible to record intracellularly and eject substances juxtacellularly during naturally occurring states of sleep and wakefulness was developed, over a period of two years, specifically to avoid the problems that are inherent in the microdialysis technique that Brooks and Peever employed. In conclusion, during wakefulness, numerous receptors on a great many neuronal elements in and in the vicinity of the trigeminal motor nucleus are normally activated in highly regulated sequences depending upon the specific behavior that is being performed, such as vocalization, biting, chewing, swallowing, etc. On the other hand, during REM sleep, only receptors on alpha motoneurons in the trigeminal motor nucleus, which are involved in state-dependent control processes, are excited. These latter receptors have been identified as glycinergic and have been shown to be activated, monosynaptically, by projections from the region of the nucleus reticularis gigantocellularis. Therefore, there is no justification for Brooks and Peever to claim that an unknown \"biochemical substrate\" is responsible for atonia during REM sleep, nor do they provide any data or reason not to continue to believe in the veracity of their initial statement, reflecting the
consensus that \"glycinergic inhibition of somatic motoneurons is responsible for loss of postural muscle tone in REM sleep\".