Abstract
THE RECENT STUDY BY BROOKS AND PEEVER1 EXAMINES STATE-DEPENDENT CHANGES IN TRIGEMINAL MOTOR ACTIVITY IN FREELY BEHAVING RATS following microdialysis of glycine and GABAA-receptor antagonists into the V nucleus. Authors challenge the concept established in the 60s2 and entrenched in the 80s primarily with the intracellular recording studies of Morales, Chase and Soja3–8 that the muscle atonia of REM sleep is produced by a common, brainstem-derived, REM or active-sleep specific, postsynaptic, glycine-mediated inhibition of somatic motoneurons.
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