Microinjection of NMDA and non-NMDA agonists into the same sites in pontomedullary motor "inhibitory" areas of decerebrate animals produced opposite effects on muscle tone. Microinjection of non-NMDA agonists into peri-locus coeruleus alpha (peri-LC alpha) and nucleus magnocellularis (NMC) suppressed muscle tone, while injection of NMDA agonists at the same sites increased muscle tone and produced locomotion. The latency, duration, and magnitude of muscle tone change after both NMDA and non-NMDA agonist injections were dose dependent. Increased muscle tone and locomotor effects were blocked by NMDA antagonists, and muscle tone suppression effects were blocked by non-NMDA antagonists. We conclude that pontomedullary non-NMDA receptors mediate muscle tone suppression, and that NMDA receptors mediate locomotion and muscle tone facilitation. Activation of both NMDA and non-NMDA pontomedullary receptors by glutamate release in REM sleep can explain the combination of motor activation and loss of muscle tone that characterizes this state. In the waking animal, the co-localization of these mechanisms may facilitate the coordination of locomotion with postural adjustments.