The motor inhibitory system operating during active sleep is tonically suppressed by GABAergic mechanisms during other states

The present study was undertaken to explore the neuronal mechanisms respons ible for muscle atonia that occurs after the microinjection of bicuculline into the nucleus pontis oralis (NPO). Specifically, we wished to test the h ypothesis that motoneurons are postsynaptically inhibited after the microin jection of bicuculline into the NPO and determine whether the inhibitory me chanisms are the same as those that are utilized during naturally occurring active (rapid eye movement) sleep. Accordingly, intracelular records were obtained from lumbar motoneurons in cats anesthetized with alpha -chloralos e before and during bicuculline-induced motor inhibition. The microinjectio n of bicuculline into the NPO resulted in a sustained reduction in the ampl itude of the spinal cord Ia-monosynaptic reflex. In addition, lumbar motone urons exhibited significant changes in their electrophysiological propertie s [i.e., a decrease in input resistance and membrane time constant, a reduc tion in the amplitude of the action potential's afterhyperpolarization (AHP ) and an increase in rheobase]. Discrete, large-amplitude inhibitory postsy naptic potentials (IPSPs) were also observed in high-gain recordings from l umbar 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 motoneuron s, as well as the development of active sleep-specific IPSPs, indicate that lumbar motoneurons are postsynaptically inhibited following the intraponti ne administration of bicuculline in a manner that is comparable to that whi ch occurs spontaneously during the atonia. of active sleep. The present res ults support the conclusion that the brain stem-spinal cord inhibitory syst em, which is responsible for motor inhibition during active sleep, can be a ctivated by the injection of bicuculline into the NPO. These data suggest t hat the active sleep-dependent motor inhibitory system is under constant GA BAergic inhibitory control, which is centered in the NPO. Thus during wakef ulness and quiet sleep, the glycinergically mediated postsynaptic inhibitio n of motoneurons is prevented from occurring due to GABAergic mechanisms.