Confirmation of the consensus that glycinergic postsynaptic inhibition is responsible for the atonia of REM sleep

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".